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        <title>Advances in Immunology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Advances in Immunology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Advances+in+Immunology&t=Advances+in+Immunology&s=Search&f=source]]></link>
        <lastBuildDate>Tue, 17 Nov 2009 13:39:01 +0100</lastBuildDate>
        <item>
            <title>Chapter 1: The physiological role of lysyl tRNA synthetase in the immune system.</title>
            <link>http://www.medworm.com/index.php?rid=2807184&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19755181%26dopt%3DAbstract</link>
            <description>Authors: Nechushtan H, Kim S, Kay G, Razin E
    Lysyl tRNA synthetase (LysRS) is an aminoacyl-tRNA synthetase (AaRS). This group of ancient proteins, known for their critical role in translation, was found in recent years to function in a variety of other roles. Besides its enzymatic activity in aminoacylation of tRNA, LysRS can produce dinucleotide diadenosine tetraphosphate (Ap(4)A). Intracellularly, it is found mainly in the cytoplasm as a part of a multisynthetase complex where it interacts with several proteins, most notably AIMP2. Besides its role in translation it has been demonstrated that LysRS can act as a cytokine-like molecule, secreted by cells and having distinct effects on macrophages. Moreover, LysRS can bind to the transcription factors USF2 and MITF and can influence the...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2807184</comments>
            <pubDate>Fri, 18 Sep 2009 17:50:02 +0100</pubDate>
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            <title>Chapter 2: Kill the bacteria...and also their messengers?</title>
            <link>http://www.medworm.com/index.php?rid=2807183&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19755182%26dopt%3DAbstract</link>
            <description>Authors: Munford R, Lu M, Varley A
    We consider here a previously neglected aspect of recovery from infectious diseases: how animals dispose of the dead microbes in their tissues. For one of the most important disease-causing microorganisms, Gram-negative bacteria, there is now evidence that the host catabolism of a key microbial molecule is essential for full recovery. As might be expected, it is the same bacterial molecule that animals sense to detect the presence of Gram-negative bacteria in their tissues, the cell wall lipopolysaccharide (LPS). Here, we discuss current knowledge about LPS sensing with emphasis on the host enzyme that inactivates this microbial &quot;messenger&quot; molecule. We also consider the possibility that the rate at which stimulatory microbial molecules undergo inacti...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2807183</comments>
            <pubDate>Fri, 18 Sep 2009 17:50:02 +0100</pubDate>
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            <title>Chapter 3: Role of SOCS in allergic and innate immune responses.</title>
            <link>http://www.medworm.com/index.php?rid=2807182&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19755183%26dopt%3DAbstract</link>
            <description>Authors: Cassel SL, Rothman PB
    Cytokines are powerful mediators of the immune response that, following initial release by components of the innate system, drive effector functions as well as stimulate the additional arms of the response. Their individual functions are diverse, with stimulatory and inhibitory actions, with the resultant systemic immune response a summation of these actions. The frequently opposing effects of cytokines determine that the blockade of one results in the functional augmentation of the other. Thus, the differential regulation of cytokines profoundly influences the character of the immune response. The suppressor of cytokine signaling proteins are a family of molecules pivotal to this critical regulation. In this review, we will discuss their structural compo...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2807182</comments>
            <pubDate>Fri, 18 Sep 2009 17:50:02 +0100</pubDate>
            <guid isPermaLink="false">2807182</guid>        </item>
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            <title>Chapter 4: Multitasking by exploitation of intracellular transport functions the many faces of FcRn.</title>
            <link>http://www.medworm.com/index.php?rid=2807180&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19755184%26dopt%3DAbstract</link>
            <description>Authors: Ward ES, Ober RJ
    The MHC Class I-related receptor, FcRn, transports antibodies of the immunoglobulin G (IgG) class within and across a diverse array of different cell types. Through this transport, FcRn serves multiple roles throughout adult life that extend well beyond its earlier defined function of transcytosing IgGs from mother to offspring. These roles include the maintenance of IgG levels and the delivery of antigen in the form of immune complexes to degradative compartments within cells. Recent studies have led to significant advances in knowledge of the intracellular trafficking of FcRn and (engineered) IgGs at both the molecular and cellular levels. The engineering of FcRn-IgG (or Fc) interactions to generate antibodies of increased longevity represents an area of act...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2807180</comments>
            <pubDate>Fri, 18 Sep 2009 17:50:02 +0100</pubDate>
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            <title>Chapter 1 Antigen Presentation by CD1 Lipids, T Cells, and NKT Cells in Microbial Immunity.</title>
            <link>http://www.medworm.com/index.php?rid=2529080&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19477319%26dopt%3DAbstract</link>
            <description>Authors: Cohen NR, Garg S, Brenner MB
    The discovery of molecules capable of presenting lipid antigens, the CD1 family, and of the T cells that recognize them, has opened a new dimensionin our understanding of cell-mediated immunity against infection. Like MHC Class I molecules, CD1 isoforms (CD1a, b, c and d) are assembled in the ER and sent to the cell surface. However, in contrast to MHC molecules, CD1 complexes are then re-internalized into specific endocytic compartments where they can bind lipid antigens. These include a broad scope of both self and foreign molecules that range from simple fatty acids or phospholipids, to more complex glycolipids, isoprenoids, mycolates and lipopeptides. Lipid-loaded CD1 molecules are then delivered to the cell surface and can be surveyed by CD1-r...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2529080</comments>
            <pubDate>Sat, 27 Jun 2009 13:08:05 +0100</pubDate>
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            <title>Chapter 2 how the immune system achieves self-nonself discrimination during adaptive immunity.</title>
            <link>http://www.medworm.com/index.php?rid=2529078&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19477320%26dopt%3DAbstract</link>
            <description>Authors: Jiang H, Chess L
    We propose an &quot;Avidity Model of Self-Nonself Discrimination&quot; in which self-nonself discrimination is achieved by both central thymic selection and peripheral immune regulation. The conceptual framework that links these two events is the understanding that both in the thymus and in the periphery the survival or the fate of T cells is determined by the avidity of the interactions between T cell receptors (TCRs) on T cells, specific to any antigens and MHC/antigen peptides presented by antigen-presenting cells (APCs). We envision that the immune system achieves self-nonself discrimination, during adaptive immunity, not by recognizing the structural differences between self versus foreign antigens, but rather by perceiving the avidity of T cell activation. Intrath...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2529078</comments>
            <pubDate>Sat, 27 Jun 2009 13:08:05 +0100</pubDate>
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            <title>Chapter 3 cellular and molecular mechanisms in atopic dermatitis.</title>
            <link>http://www.medworm.com/index.php?rid=2529076&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19477321%26dopt%3DAbstract</link>
            <description>Authors: Oyoshi MK, He R, Kumar L, Yoon J, Geha RS
    Atopic dermatitis (AD) is a pruritic inflammatory skin disease associated with a personal or family history of allergy. The prevalence of AD is on the rise and estimated at approximately 17% in the USA. The fundamental lesion in AD is a defective skin barrier that results in dry itchy skin, and is aggravated by mechanical injury inflicted by scratching. This allows entry of antigens via the skin and creates a milieu that shapes the immune response to these antigens. This review discusses recent advances in our understanding of the abnormal skin barrier in AD, namely abnormalities in epidermal structural proteins, such as filaggrin, mutated in approximately 15% of patients with AD, epidermal lipids, and epidermal proteases and protease ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2529076</comments>
            <pubDate>Sat, 27 Jun 2009 13:08:05 +0100</pubDate>
            <guid isPermaLink="false">2529076</guid>        </item>
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            <title>Chapter 4 micromanagers of immune cell fate and function.</title>
            <link>http://www.medworm.com/index.php?rid=2529074&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19477322%26dopt%3DAbstract</link>
            <description>Authors: Petrocca F, Lieberman J
    MicroRNAs (miRNAs) regulate cell fate during development and in response to environmental cues. Here, we review the emerging story of how miRNAs regulate immune cell development and function.
    PMID: 19477322 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2529074</comments>
            <pubDate>Sat, 27 Jun 2009 13:08:05 +0100</pubDate>
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            <title>Chapter 5 immune pathways for translating viral infection into chronic airway disease.</title>
            <link>http://www.medworm.com/index.php?rid=2529072&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19477323%26dopt%3DAbstract</link>
            <description>Authors: Holtzman MJ, Byers DE, Benoit LA, Battaile JT, You Y, Agapov E, Park C, Grayson MH, Kim EY, Patel AC
    To better understand the immune basis for chronic inflammatory lung disease, we analyzed a mouse model of lung disease that develops after respiratory viral infection. The disease that develops in this model is similar to asthma and chronic obstructive pulmonary disease (COPD) in humans and is manifested after the inciting virus has been cleared to trace levels. The model thereby mimics the relationship of paramyxoviral infection to the development of childhood asthma in humans. When the acute lung disease appears in this model (at 3 weeks after viral inoculation), it depends on an immune axis that is initiated by expression and activation of the high-affinity IgE receptor (Fcv...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2529072</comments>
            <pubDate>Sat, 27 Jun 2009 13:08:05 +0100</pubDate>
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        <item>
            <title>Chapter 1 TSLP in Epithelial Cell and Dendritic Cell Cross Talk.</title>
            <link>http://www.medworm.com/index.php?rid=2210031&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19231591%26dopt%3DAbstract</link>
            <description>Authors: Liu YJ
    Dendritic cells (DCs) are professional antigen-presenting cells that have the ability to sense infection and tissue stress, sample and present antigen to T lymphocytes, and instruct the initiation of different forms of immunity and tolerance. The functional versatility of DCs depends on their remarkable ability to translate collectively the information from the invading microbes, as well as their resident tissue microenvironments. Recent progress in understanding Toll-like receptor (TLR) biology has illuminated the mechanisms by which DCs link innate and adaptive antimicrobial immune responses. However, how tissue microenvironments shape the function of DCs has remained elusive. Recent studies of TSLP (thymic stromal lymphopoietin), an epithelial cell-derived cytokine t...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2210031</comments>
            <pubDate>Tue, 24 Feb 2009 20:27:01 +0100</pubDate>
            <guid isPermaLink="false">2210031</guid>        </item>
        <item>
            <title>Chapter 2 natural killer cell tolerance licensing and other mechanisms.</title>
            <link>http://www.medworm.com/index.php?rid=2210030&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19231592%26dopt%3DAbstract</link>
            <description>Authors: Jonsson AH, Yokoyama WM
    Armed with potent cytotoxic and immunostimulatory effector functions, natural killer (NK) cells have the potential to cause significant damage to normal self cells unless controlled by self-tolerance mechanisms. NK cells identify and attack target cells based on integration of signals from activation and inhibitory receptors, whose ligands exhibit complex expression and/or binding patterns. Preservation of NK cell self-tolerance must therefore go beyond mere engagement of inhibitory receptors during effector functions. Herein, we review recent work that has uncovered a number of mechanisms to ensure self-tolerance of NK cells. For example, licensing of NK cells allows only NK cells that can engage self-MHC to become functionally competent, or licensed. ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2210030</comments>
            <pubDate>Tue, 24 Feb 2009 20:27:01 +0100</pubDate>
            <guid isPermaLink="false">2210030</guid>        </item>
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            <title>Chapter 3 biology of the eosinophil.</title>
            <link>http://www.medworm.com/index.php?rid=2210029&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19231593%26dopt%3DAbstract</link>
            <description>Authors: Blanchard C, Rothenberg ME
    In this review, we aim to put in perspective the biology of a multifunctional leukocyte, the eosinophil, by placing it in the context of innate and adaptive immune responses. Eosinophils have a unique contribution in initiating inflammatory and adaptive responses, due to their bidirectional interactions with dendritic cells and T cells, as well as their large panel of secreted cytokines and soluble mediators. The mechanisms and consequences of eosinophil responses in experimental inflammatory models and human diseases are discussed.
    PMID: 19231593 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2210029</comments>
            <pubDate>Tue, 24 Feb 2009 20:27:01 +0100</pubDate>
            <guid isPermaLink="false">2210029</guid>        </item>
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            <title>Chapter 4 basophils beyond effector cells of allergic inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=2210028&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19231594%26dopt%3DAbstract</link>
            <description>Authors: Schroeder JT
    Despite being first described in humans nearly 130 years ago, the basophil granulocyte has received little recognition other than being the least common leukocyte circulating in blood. Even after its identity as the source of histamine released by blood cells in response to reaginic IgE, its role in allergic disease has largely been viewed as redundant to that of the tissue mast cell. This line of thought, however, is changing with evidence that has emerged during the last 15 years. Not only have these rare cells been shown to constitute a significant source of cytokines (IL-4 and IL-13) vital to the pathogenesis of allergic disease, but by doing so, may very well modulate T-helper 2-type inflammation at the level of T-cell/dendritic cell interactions. This novel ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2210028</comments>
            <pubDate>Tue, 24 Feb 2009 20:27:01 +0100</pubDate>
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            <title>Chapter 5 DNA Targets of AID Evolutionary Link Between Antibody Somatic Hypermutation and Class Switch Recombination.</title>
            <link>http://www.medworm.com/index.php?rid=2210027&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19231595%26dopt%3DAbstract</link>
            <description>We describe properties of the S sequences, and discuss species and isotypic differences among S regions. Common properties of SHM and CSR target sequences suggest that evolution of S regions might involve the duplication and selection of SHM hotspots.
    PMID: 19231595 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2210027</comments>
            <pubDate>Tue, 24 Feb 2009 20:27:01 +0100</pubDate>
            <guid isPermaLink="false">2210027</guid>        </item>
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            <title>Chapter 6 interleukin 5 in the link between the innate and acquired immune response.</title>
            <link>http://www.medworm.com/index.php?rid=2210026&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19231596%26dopt%3DAbstract</link>
            <description>Authors: Takatsu K, Kouro T, Nagai Y
    Interleukin-5 (IL-5) is an interdigitating homodimeric glycoprotein that is initially identified by its ability to support the in vitro growth and differentiation of mouse B cells and eosinophils. IL-5 transgenic mouse shows two predominant features, remarkable increase in B-1 cells resulting in enhanced serum antibody levels, predominantly IgM, IgA, and IgE classes and in expansion of eosinophil numbers in the blood and eosinophil infiltration into various tissues. Conversely, mice lacking a functional gene for IL-5 or IL-5 receptor alpha chain (IL-5Ralpha) display a number of developmental and functional impairments in B cells and eosinophils. IL-5 receptor (IL-5R) comprises alpha and betac chains. IL-5 specifically binds to IL-5Ralpha and induces...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2210026</comments>
            <pubDate>Tue, 24 Feb 2009 20:27:01 +0100</pubDate>
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            <title>Chapter 1 immune regulation by B cells and antibodies a view towards the clinic.</title>
            <link>http://www.medworm.com/index.php?rid=1770370&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18772002%26dopt%3DAbstract</link>
            <description>Authors: Hoehlig K, Lampropoulou V, Roch T, Neves P, Calderon-Gomez E, Anderton SM, Steinhoff U, Fillatreau S
    B lymphocytes contribute to immunity in multiple ways, including production of antibodies, presentation of antigen to T cells, organogenesis of secondary lymphoid organs, and secretion of cytokines. Recent clinical trials have shown that depleting B cells can be highly beneficial for patients with autoimmune diseases, implicating B cells and antibodies as key drivers of pathology. However, it should be kept in mind that B cell responses and antibodies also have important regulatory roles in limiting autoimmune pathology. Here, we analyze clinical examples illustrating the potential of antibodies as treatment for immune-mediated disorders and discuss the underlying mechanisms. F...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1770370</comments>
            <pubDate>Sun, 07 Sep 2008 10:00:23 +0100</pubDate>
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            <title>Chapter 2 cumulative environmental changes, skewed antigen exposure, and the increase of allergy.</title>
            <link>http://www.medworm.com/index.php?rid=1770369&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18772003%26dopt%3DAbstract</link>
            <description>Authors: Chang TW, Pan AY
    The human immune system evolved over many hundreds of million of years in the ancestors of vertebrates and mammals to defend them against infectious and parasitic organisms in their natural habitats. By the time the Primates and Rodentia orders diverged about 88 million years ago, the human immune system was largely configured. From about 125,000 years ago, marked by the use of fire, Homo sapiens began to make substantial changes in their living environment and lifestyle. Here, we examine those changes in two phases, before and after the Industrial Revolution, and analyze their impact on the exposure of our immune system to infectious organisms and to harmless environmental antigens. Our analyses show that the cumulative changes in environment and lifestyle in...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1770369</comments>
            <pubDate>Sun, 07 Sep 2008 10:00:23 +0100</pubDate>
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            <title>Chapter 3 New Insights on Mast Cell Activation via the High Affinity Receptor for IgE.</title>
            <link>http://www.medworm.com/index.php?rid=1770368&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18772004%26dopt%3DAbstract</link>
            <description>Authors: Rivera J, Fierro NA, Olivera A, Suzuki R
    Mast cells are innate immune cells that function as regulatory or effector cells and serve to amplify adaptive immunity. In adaptive immunity these cells function primarily through cell surface Fc receptors that bind immunoglobulin antibodies. The dysregulation of their adaptive role makes them central players in allergy and asthma. Upon encountering an allergen (antigen), which is recognized by immunoglobulin E (IgE) antibodies bound to the high affinity IgE receptor (FcvarepsilonRI) expressed on their cell surface, mast cells secrete both preformed and newly synthesized mediators of the allergic response. Blocking of these responses is an objective in therapeutic intervention of allergic diseases. Thus, understanding the mechanisms by...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1770368</comments>
            <pubDate>Sun, 07 Sep 2008 10:00:23 +0100</pubDate>
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            <title>Chapter 4 B cells and autoantibodies in the pathogenesis of multiple sclerosis and related inflammatory demyelinating diseases.</title>
            <link>http://www.medworm.com/index.php?rid=1770367&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18772005%26dopt%3DAbstract</link>
            <description>Authors: McLaughlin KA, Wucherpfennig KW
    Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). The mainstream view is that MS is caused by an autoimmune attack of the CNS myelin by myelin-specific CD4 T cells, and this perspective is supported by extensive work in the experimental autoimmune encephalomyelitis (EAE) model of MS as well as immunological and genetic studies in humans. However, it is important to keep in mind that other cell populations of the immune system are also essential in the complex series of events leading to MS, as exemplified by the profound clinical efficacy of B cell depletion with Rituximab. This review discusses the mechanisms by which B cells contribute to the pathogenesis of MS and dissects their role ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1770367</comments>
            <pubDate>Sun, 07 Sep 2008 10:00:23 +0100</pubDate>
            <guid isPermaLink="false">1770367</guid>        </item>
        <item>
            <title>Chapter 5 human B cell subsets.</title>
            <link>http://www.medworm.com/index.php?rid=1770366&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18772006%26dopt%3DAbstract</link>
            <description>Authors: Jackson SM, Wilson PC, James JA, Capra JD
    
    PMID: 18772006 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1770366</comments>
            <pubDate>Sun, 07 Sep 2008 10:00:23 +0100</pubDate>
            <guid isPermaLink="false">1770366</guid>        </item>
        <item>
            <title>T Cell Activation and the Cytoskeleton: You Can't Have One Without the Other.</title>
            <link>http://www.medworm.com/index.php?rid=1469486&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18501768%26dopt%3DAbstract</link>
            <description>Authors: Gomez TS, Billadeau DD
    More than a quarter of a century has passed since the observation that T cells rapidly polarize their actin and microtubule cytoskeletal systems toward antigen-presenting cells during activation. Since this initial discovery, several receptors on T cells (e.g., T cell receptor [TCR], co-receptors, integrins, and chemokine receptors) have been identified to regulate these two cytoskeletal networks through complex signaling pathways, which are still being elucidated. There is now an undeniable body of biochemical, pharmacological, and genetic evidence indicating that regulators of actin and microtubule dynamics are crucial for T cell activation and effector functions. In fact, the actin cytoskeleton participates in the initial clustering of TCR-major histo...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1469486</comments>
            <pubDate>Tue, 27 May 2008 16:20:06 +0100</pubDate>
            <guid isPermaLink="false">1469486</guid>        </item>
        <item>
            <title>HLA Class II Transgenic Mice Mimic Human Inflammatory Diseases.</title>
            <link>http://www.medworm.com/index.php?rid=1469485&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18501769%26dopt%3DAbstract</link>
            <description>Authors: Mangalam AK, Rajagopalan G, Taneja V, David CS
    Population studies have shown that among all the genetic factors linked with autoimmune disease development, MHC class II genes on chromosome 6 accounts for majority of familial clustering in the common autoimmune diseases. Despite the highly polymorphic nature of HLA class II genes, majority of autoimmune diseases are linked to a limited set of class II-DR or -DQ alleles. Thus a more detailed study of these HLA-DR and -DQ alleles were needed to understand their role in genetic predisposition and pathogenesis of autoimmune diseases. Although in vitro studies using class-II restricted CD4 T cells and purified class II molecules have helped us in understanding some aspects of HLA class-II association with disease, it is difficult to...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1469485</comments>
            <pubDate>Tue, 27 May 2008 16:20:06 +0100</pubDate>
            <guid isPermaLink="false">1469485</guid>        </item>
        <item>
            <title>Roles of Zinc and Zinc Signaling in Immunity: Zinc as an Intracellular Signaling Molecule.</title>
            <link>http://www.medworm.com/index.php?rid=1469484&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18501770%26dopt%3DAbstract</link>
            <description>Authors: Hirano T, Murakami M, Fukada T, Nishida K, Yamasaki S, Suzuki T
    Zinc (Zn) is an essential nutrient required for cell growth, differentiation, and survival, and its deficiency causes growth retardation, immunodeficiency, and other health problems. Therefore, Zn homeostasis must be tightly controlled in individual cells. Zn is known to be important in the immune system, although its precise roles and mechanisms have not yet been resolved. Zn has been suggested to act as a kind of neurotransmitter. In addition, Zn has been shown to bind and affect the activity of several signaling molecules, such as protein tyrosine phosphatases (PTPs). However, it has not been known whether Zn itself might act as an intracellular signaling molecule, that is, a molecule whose intracellular status...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1469484</comments>
            <pubDate>Tue, 27 May 2008 16:20:06 +0100</pubDate>
            <guid isPermaLink="false">1469484</guid>        </item>
        <item>
            <title>The SLAM and SAP Gene Families Control Innate and Adaptive Immune Responses.</title>
            <link>http://www.medworm.com/index.php?rid=1469483&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18501771%26dopt%3DAbstract</link>
            <description>Authors: Calpe S, Wang N, Romero X, Berger SB, Lanyi A, Engel P, Terhorst C
    The nine SLAM-family genes, SLAMF1-9, a subfamily of the immunoglobulin superfamily, encode differentially expressed cell-surface receptors of hematopoietic cells. Engagement with their ligands, which are predominantly homotypic, leads to distinct signal transduction events, for instance those that occur in the T or NK cell immune synapse. Upon phosphorylation of one or more copies of a unique tyrosine-based signaling motif in their cytoplasmic tails, six of the SLAM receptors recruit the highly specific single SH2-domain adapters SLAM-associated protein (SAP), EAT-2A, and/or EAT-2B. These adapters in turn bind to the tyrosine kinase Fyn and/or other protein tyrosine kinases connecting the receptors to signal t...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1469483</comments>
            <pubDate>Tue, 27 May 2008 16:20:06 +0100</pubDate>
            <guid isPermaLink="false">1469483</guid>        </item>
        <item>
            <title>Conformational Plasticity and Navigation of Signaling Proteins in Antigen-Activated B Lymphocytes.</title>
            <link>http://www.medworm.com/index.php?rid=1469482&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18501772%26dopt%3DAbstract</link>
            <description>Authors: Engels N, Engelke M, Wienands J
    Over the past two decades our view of the B cell antigen receptor (BCR) has fundamentally changed. Being initially regarded as a mute antibody orphan of the B cell surface, the BCR turned out to be a complex multimolecular machine monitoring almost all stages of B cell development, selection, and activation through a plethora of ubiquitously and cell-type-specific effector proteins. A comprehensive understanding of the many BCR signaling facets is still out but a few common biochemical principles outlined in this review operate at the level of receptor activation and orchestrate specific wiring of intracellular transducer cascades. First, initiation and processing of antigen-induced signal transduction relies on transient conformational changes ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1469482</comments>
            <pubDate>Tue, 27 May 2008 16:20:06 +0100</pubDate>
            <guid isPermaLink="false">1469482</guid>        </item>
        <item>
            <title>New insights into adaptive immunity in chronic neuroinflammation.</title>
            <link>http://www.medworm.com/index.php?rid=1007060&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981203%26dopt%3DAbstract</link>
            <description>Authors: Siffrin V, Brandt AU, Herz J, Zipp F
    Understanding the immune response in the central nervous system (CNS) is crucial for the development of new therapeutic concepts in chronic neuroinflammation, which differs considerably from other autoimmune diseases. Special immunologic properties of inflammatory processes in the CNS, which is often referred to as an immune privileged site, imply distinct features of CNS autoimmune disease in terms of disease initiation, perpetuation, and therapeutic accessibility. Furthermore, the CNS is a stress-sensitive organ with a low capacity for self-renewal and is highly prone to bystander damage caused by CNS inflammation. This leads to neuronal degeneration that contributes considerably to the phenotype of the disease. In this chapter, we discus...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1007060</comments>
            <pubDate>Tue, 06 Nov 2007 14:24:31 +0100</pubDate>
            <guid isPermaLink="false">1007060</guid>        </item>
        <item>
            <title>Regulation of Interferon-gamma During Innate and Adaptive Immune Responses.</title>
            <link>http://www.medworm.com/index.php?rid=1007059&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981204%26dopt%3DAbstract</link>
            <description>Authors: Schoenborn JR, Wilson CB
    Interferon-gamma (IFN-gamma) is crucial for immunity against intracellular pathogens and for tumor control. However, aberrant IFN-gamma expression has been associated with a number of autoinflammatory and autoimmune diseases. This cytokine is produced predominantly by natural killer (NK) and natural killer T (NKT) cells as part of the innate immune response, and by Th1 CD4 and CD8 cytotoxic T lymphocyte (CTL) effector T cells once antigen-specific immunity develops. Herein, we briefly review the functions of IFN-gamma, the cells that produce it, the cell extrinsic signals that induce its production and influence the differentiation of na&amp;#xEF;ve T cells into IFN-gamma-producing effector T cells, and the signaling pathways and transcription factors that...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1007059</comments>
            <pubDate>Tue, 06 Nov 2007 14:24:31 +0100</pubDate>
            <guid isPermaLink="false">1007059</guid>        </item>
        <item>
            <title>The expansion and maintenance of antigen-selected CD8(+) T cell clones.</title>
            <link>http://www.medworm.com/index.php?rid=1007058&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981205%26dopt%3DAbstract</link>
            <description>Authors: Fearon DT
    The biological purpose of the mature, postthymic CD8(+) T cell is to respond to microbial antigens with a developmental program of clonal expansion and concomitant differentiation leading to effector cells (T(EFF)) that provide antimicrobial defense. Because many microbial infections persist into a chronic phase, this antigen-stimulated developmental program must be capable of continually generating T(EFF), perhaps for the lifetime of the individual. This chapter proposes that the ability of a CD8(+) T cell clone to maintain the continual production of T(EFF) during periods of persistent antigenic stimulation is based on a program that has two sequential phases of clonal expansion: an initial stage that occurs mainly in the secondary lymphoid tissues and is mediated ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1007058</comments>
            <pubDate>Tue, 06 Nov 2007 14:24:31 +0100</pubDate>
            <guid isPermaLink="false">1007058</guid>        </item>
        <item>
            <title>Inherited Complement Regulatory Protein Deficiency Predisposes to Human Disease in Acute Injury and Chronic Inflammatory StatesThe Examples of Vascular Damage in Atypical Hemolytic Uremic Syndrome and Debris Accumulation in Age-Related Macular Degeneration.</title>
            <link>http://www.medworm.com/index.php?rid=1007057&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981206%26dopt%3DAbstract</link>
            <description>Authors: Richards A, Kavanagh D, Atkinson JP
    In this chapter, we examine the role of complement regulatory activity in atypical hemolytic uremic syndrome (aHUS) and age-related macular degeneration (AMD). These diseases are representative of two distinct types of complement-mediated injury, one being acute and self-limited, the other reflecting accumulation of chronic damage. Neither condition was previously thought to have a pathologic relationship to the immune system. However, alterations in complement regulatory protein genes have now been identified as major predisposing factors for the development of both diseases. In aHUS, heterozygous mutations leading to haploinsufficiency and function-altering polymorphisms in complement regulators have been identified, while in AMD, polymorp...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1007057</comments>
            <pubDate>Tue, 06 Nov 2007 14:24:31 +0100</pubDate>
            <guid isPermaLink="false">1007057</guid>        </item>
        <item>
            <title>Fc-Receptors as Regulators of Immunity.</title>
            <link>http://www.medworm.com/index.php?rid=1007056&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981207%26dopt%3DAbstract</link>
            <description>Authors: Nimmerjahn F, Ravetch JV
    Receptors for immunoglobulins [Fc-receptors (FcRs)] are widely expressed throughout the immune system. By binding to the antibody Fc-portion, they provide a link between the specificity of the adaptive immune system and the powerful effector functions triggered by innate immune effector cells. By virtue of coexpression of activating and inhibitory FcRs on the same cell, they set a threshold for immune cell activation by immune complexes (ICs). Besides their involvement in the efferent phase of an immune response, they are also important for modulating adaptive immune responses by regulating B cell and dendritic cell (DC) activation. Deletion of the inhibitory FcR leads to the loss of tolerance in the humoral immune system and the development of autoimm...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1007056</comments>
            <pubDate>Tue, 06 Nov 2007 14:24:31 +0100</pubDate>
            <guid isPermaLink="false">1007056</guid>        </item>
        <item>
            <title>Fate decisions regulating bone marrow and peripheral B lymphocyte development.</title>
            <link>http://www.medworm.com/index.php?rid=882352&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17869609%26dopt%3DAbstract</link>
            <description>Authors: Monroe JG, Dorshkind K
    In adult mammals, bone marrow pluripotent hematopoietic stem cells generate B lymphoid-specified progeny that progress through a series of well-characterized stages before generating B-cell receptor expressing B lymphocytes. These functionally immature B lymphocytes then migrate to the spleen wherein they differentiate through transitional stages into follicular or marginal zone B lymphocytes capable of responding to T-dependent and -independent antigens, respectively. During the terminal stages of B lymphocyte development in the bone marrow, as well as immediately following egress into the peripheral compartments, B lymphocytes are counterselected to eliminate B lymphocytes with potentially dangerous self-reactivity. These developmental and selection ev...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882352</comments>
            <pubDate>Wed, 19 Sep 2007 01:06:19 +0100</pubDate>
            <guid isPermaLink="false">882352</guid>        </item>
        <item>
            <title>Tolerance and autoimmunity: lessons at the bedside of primary immunodeficiencies.</title>
            <link>http://www.medworm.com/index.php?rid=882351&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17869610%26dopt%3DAbstract</link>
            <description>Authors: Carneiro-Sampaio M, Coutinho A
    The recent progress in the genetic characterization of many primary immunodeficiencies (PIDs) allows for a better understanding of immune molecular and cellular mechanisms. The present chapter discusses associations between PIDs and autoimmune diseases (AIDs) in this new light. PIDs are classified according to the frequency of association with AIDs, defining four groups of conditions: systematic (more than 80% of all patients), strong (10-80%), mild (less than 10%), and absent (no available descriptions). Several general conclusions could be drawn: (1) pathological autoimmune (AI) manifestations are very frequently associated with PIDs, indicating that, contrary to conventional notions, antimicrobial protection and natural tolerance to body tissu...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882351</comments>
            <pubDate>Wed, 19 Sep 2007 01:06:19 +0100</pubDate>
            <guid isPermaLink="false">882351</guid>        </item>
        <item>
            <title>B-cell self-tolerance in humans.</title>
            <link>http://www.medworm.com/index.php?rid=882350&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17869611%26dopt%3DAbstract</link>
            <description>Authors: Wardemann H, Nussenzweig MC
    Two mechanisms account for generation of the human antibody repertoire; V(D)J recombination during the early stages of B-cell development in the bone marrow and somatic mutation of immunoglobulin genes in mature B cells responding to antigen in the periphery. V(D)J recombination produces diversity by random joining of gene segments and somatic mutation by introducing random point mutations. Both are required to attain the degree of antigen receptor diversification that is necessary for immune protection: defects in either mechanism are associated with increased susceptibility to infection. However, the downside of producing enormous random diversity in the antibody repertoire is the generation of autoantibodies. To prevent autoimmunity B cells expre...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882350</comments>
            <pubDate>Wed, 19 Sep 2007 01:06:19 +0100</pubDate>
            <guid isPermaLink="false">882350</guid>        </item>
        <item>
            <title>Manipulation of Regulatory T-Cell Number and Function with CD28-Specific Monoclonal Antibodies.</title>
            <link>http://www.medworm.com/index.php?rid=882349&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17869612%26dopt%3DAbstract</link>
            <description>Authors: H&amp;#xFC;nig T
    Suppressor or &quot;regulatory&quot; CD4 T cells play a key role in the control of autoimmunity and overshooting immune responses to foreign antigens, but can also obstruct effective anticancer therapies. The homeostasis and activation of these regulatory T cells (Treg cells) is tightly connected to that of effector CD4 T cells via the costimulatory receptor CD28 and the cytokine IL-2: Both subsets require costimulation to be activated by antigen, and Treg cells additionally depend on IL-2 produced by effector CD4 T cells in a costimulation-dependent fashion. Depending on the therapeutic aim, blockade, or stimulation of CD28 with monoclonal antibodies (mAb) can therefore profoundly affect the size and activity of the Treg compartment. In this chapter, experiments performed ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882349</comments>
            <pubDate>Wed, 19 Sep 2007 01:06:19 +0100</pubDate>
            <guid isPermaLink="false">882349</guid>        </item>
        <item>
            <title>Osteoimmunology: a view from the bone.</title>
            <link>http://www.medworm.com/index.php?rid=882348&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17869613%26dopt%3DAbstract</link>
            <description>Authors: David JP
    Osteoimmunology can be defined in a very broad sense as the field of research focusing on interrelations between bone and the immune system. This is a rather opened field that covers at least three different issues. The first one is developmental, that is, organogenesis of the bones and immune systems. The second is post-developmental, that is, the role of the bone in the regulation of the immune response and role of the immune cells on the regulation of bone homeostasis. The third one is related to pathologies: Can immune cells be involved in the development of bone-related pathology? Can deregulation of the bone be causing immune-related diseases? I will not review in detail the bibliography covering osteoimmunology. This has been extensively done in Immunological R...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882348</comments>
            <pubDate>Wed, 19 Sep 2007 01:06:19 +0100</pubDate>
            <guid isPermaLink="false">882348</guid>        </item>
        <item>
            <title>Mast cell proteases.</title>
            <link>http://www.medworm.com/index.php?rid=882347&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17869614%26dopt%3DAbstract</link>
            <description>Authors: Pejler G, Abrink M, Ringvall M, Wernersson S
    Mast cells (MCs) are traditionally thought of as a nuisance for its host, for example, by causing many of the symptoms associated with allergic reactions. In addition, recent research has put focus on MCs for displaying harmful effects during various autoimmune disorders. On the other hand, MCs can also be beneficial for its host, for example, by contributing to the defense against insults such as bacteria, parasites, and snake venom toxins. When the MC is challenged by an external stimulus, it may respond by degranulation. In this process, a number of powerful preformed inflammatory &quot;mediators&quot; are released, including cytokines, histamine, serglycin proteoglycans, and several MC-specific proteases: chymases, tryptases, and carboxyp...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=882347</comments>
            <pubDate>Wed, 19 Sep 2007 01:06:19 +0100</pubDate>
            <guid isPermaLink="false">882347</guid>        </item>
        <item>
            <title>Preface.</title>
            <link>http://www.medworm.com/index.php?rid=673860&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560269%26dopt%3DAbstract</link>
            <description>Authors: Alt FW, Honjo T
    
    PMID: 17560269 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673860</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673860</guid>        </item>
        <item>
            <title>Discovery of activation-induced cytidine deaminase, the engraver of antibody memory.</title>
            <link>http://www.medworm.com/index.php?rid=673859&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560270%26dopt%3DAbstract</link>
            <description>Authors: Muramatsu M, Nagaoka H, Shinkura R, Begum NA, Honjo T
    Discovery of activation-induced cytidine deaminase (AID) paved a new path to unite two genetic alterations induced by antigen stimulation; class switch recombination (CSR) and somatic hypermutation (SHM). AID is now established to cleave specific target DNA and to serve as engraver of these genetic alterations. AID of a 198-residue protein has four important domains: nuclear localization signal and SHM-specific region at the N-terminus; the alpha-helical segment (residue 47-54) responsible for dimerization; catalytic domain (residues 56-94) shared by all the other cytidine deaminase family members; and nuclear export signal overlapping with class switch-specific domain at the C-terminus. Two alternative models have been pro...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673859</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673859</guid>        </item>
        <item>
            <title>DNA Deamination in Immunity: AID in the Context of Its APOBEC Relatives.</title>
            <link>http://www.medworm.com/index.php?rid=673858&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560271%26dopt%3DAbstract</link>
            <description>Authors: Conticello SG, Langlois MA, Yang Z, Neuberger MS
    The activation-induced cytidine deaminase (AID)/apolipoprotein B RNA-editing catalytic component (APOBEC) family is a vertebrate-restricted subgrouping of a superfamily of zinc (Zn)-dependent deaminases that has members distributed throughout the biological world. AID and APOBEC2 are the oldest family members with APOBEC1 and the APOBEC3s being later arrivals restricted to placental mammals. Many AID/APOBEC family members exhibit cytidine deaminase activity on polynucleotides, although in different physiological contexts. Here, we examine the AID/APOBEC proteins in the context of the entire Zn-dependent deaminase superfamily. On the basis of secondary structure predictions, we propose that the cytosine and tRNA deaminases are li...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673858</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673858</guid>        </item>
        <item>
            <title>The role of activation-induced deaminase in antibody diversification and chromosome translocations.</title>
            <link>http://www.medworm.com/index.php?rid=673857&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560272%26dopt%3DAbstract</link>
            <description>Authors: Ramiro A, San-Martin BR, McBride K, Jankovic M, Barreto V, Nussenzweig A, Nussenzweig MC
    Although B and T lymphocytes are similar in many respects including diversification of their antigen receptor genes by V(D)J recombination, 95% of all lymphomas diagnosed in the western world are of B-cell origin. Many of these are derived from mature B cells [Kuppers, R. (2005). Mechanisms of B-cell lymphoma pathogenesis. Nat. Rev. Cancer 5, 251-262] and display hallmark chromosome translocations involving immunoglobulin genes and a proto-oncogene partner whose expression becomes deregulated as a result of the translocation reaction [Kuppers, R. (2005). Mechanisms of B-cell lymphoma pathogenesis. Nat. Rev. Cancer 5, 251-262; Kuppers, R., and Dalla-Favera, R. (2001). Mechanisms of chromoso...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673857</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673857</guid>        </item>
        <item>
            <title>Targeting of AID-Mediated Sequence Diversification by cis-Acting Determinants.</title>
            <link>http://www.medworm.com/index.php?rid=673856&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560273%26dopt%3DAbstract</link>
            <description>Authors: Yang SY, Schatz DG
    After their assembly by V(D)J recombination, immunoglobulin (Ig) genes undergo somatic hypermutation, gene conversion, and class switch recombination to generate additional antibody diversity. The three diversification processes depend on activation-induced cytidine deaminase (AID) and are tightly linked to transcription. The reactions occur primarily on Ig genes and the molecular mechanisms that underlie their targeting to Ig loci have been of intense interest. In this chapter, we discuss the evidence linking transcription and transcriptional control elements to the three diversification pathways, and we consider how various features of chromatin could render parts of the genome permissive for AID-mediated sequence diversification.
    PMID: 17560273 [PubMe...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673856</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673856</guid>        </item>
        <item>
            <title>AID-Initiated Purposeful Mutations in Immunoglobulin Genes.</title>
            <link>http://www.medworm.com/index.php?rid=673855&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560274%26dopt%3DAbstract</link>
            <description>Authors: Goodman MF, Scharff MD, Romesberg FE
    Exposure brings risk to all living organisms. Using a remarkably effective strategy, higher vertebrates mitigate risk by mounting a complex and sophisticated immune response to counter the potentially toxic invasion by a virtually limitless army of chemical and biological antagonists. Mutations are almost always deleterious, but in the case of antibody diversification there are mutations occurring at hugely elevated rates within the variable (V) and switch regions (SR) of the immunoglobulin (Ig) genes that are responsible for binding to and neutralizing foreign antigens throughout the body. These mutations are truly purposeful. This chapter is centered on activation-induced cytidine deaminase (AID). AID is required for initiating somatic hy...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673855</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673855</guid>        </item>
        <item>
            <title>Evolution of the immunoglobulin heavy chain class switch recombination mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=673854&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560275%26dopt%3DAbstract</link>
            <description>We present a model for CSR in which transcription through S regions provides DNA substrates on which AID can generate DSB-inducing lesions. We also discuss how phosphorylation of AID may mediate interactions with cofactors that facilitate access to transcribed S regions during CSR and transcribed variable regions during the related process of somatic hypermutation (SHM). Finally, in the context of this CSR model, we further discuss current findings that suggest synapsis and joining of S region DSBs during CSR have evolved to exploit general mechanisms that function to join widely separated chromosomal DSBs.
    PMID: 17560275 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673854</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673854</guid>        </item>
        <item>
            <title>Beyond SHM and CSR: AID and Related Cytidine Deaminases in the Host Response to Viral Infection.</title>
            <link>http://www.medworm.com/index.php?rid=673853&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560276%26dopt%3DAbstract</link>
            <description>Authors: Rosenberg BR, Papavasiliou FN
    As the primary effector of immunoglobulin somatic hypermutation (SHM) and class switch recombination (CSR), activation-induced cytidine deaminase (AID) serves an important function in the adaptive immune response. Recent advances have demonstrated that AID and a group of closely related cytidine deaminases, the APOBEC3 proteins, also act in the innate host response to viral infection. Antiviral activity was first attributed to APOBEC3G as a potent inhibitor of HIV. It is now apparent that the targets of the APOBEC3 proteins extend beyond HIV, with family members acting against a wide variety of viruses as well as host-encoded retrotransposable genetic elements. Although it appears to function through a different mechanism, AID also possesses antiv...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673853</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673853</guid>        </item>
        <item>
            <title>Role of AID in Tumorigenesis.</title>
            <link>http://www.medworm.com/index.php?rid=673852&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560277%26dopt%3DAbstract</link>
            <description>Authors: Okazaki IM, Kotani A, Honjo T
    A hallmark of mature B-cell lymphomas is reciprocal chromosomal translocations involving the Ig locus and a proto-oncogene, which usually result in the deregulated, constitutive expression of the translocated gene. In addition to such translocations, proto-oncogenes are frequently hypermutated in germinal center (GC)-derived B-cell lymphomas. Although aberrant, mistargeted class switch recombination (CSR) and somatic hypermutation (SHM) events have long been suspected of causing chromosomal translocations and mutations in oncogenes, and thus of playing a critical role in the pathogenesis of most B-cell lymphomas, the molecular basis for such deregulation of CSR and SHM is only beginning to be elucidated by recent genetic approaches. The tumorigeni...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673852</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673852</guid>        </item>
        <item>
            <title>Pathophysiology of B-Cell Intrinsic Immunoglobulin Class Switch Recombination Deficiencies.</title>
            <link>http://www.medworm.com/index.php?rid=673851&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17560278%26dopt%3DAbstract</link>
            <description>Authors: Durandy A, Taubenheim N, Peron S, Fischer A
    B-cell intrinsic immunoglobulin class switch recombination (Ig-CSR) deficiencies, previously termed hyper-IgM syndromes, are genetically determined conditions characterized by normal or elevated serum IgM levels and an absence or very low levels of IgG, IgA, and IgE. As a function of the molecular mechanism, the defective CSR is variably associated to a defect in the generation of somatic hypermutations (SHMs) in the Ig variable region. The study of Ig-CSR deficiencies contributed to a better delineation of the mechanisms underlying CSR and SHM, the major events of antigen-triggered antibody maturation. Four Ig-CSR deficiency phenotypes have been so far reported: the description of the activation-induced cytidine deaminase (AID) defi...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=673851</comments>
            <pubDate>Sun, 17 Jun 2007 08:03:12 +0100</pubDate>
            <guid isPermaLink="false">673851</guid>        </item>
        <item>
            <title>Class switch recombination: a comparison between mouse and human.</title>
            <link>http://www.medworm.com/index.php?rid=504196&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17383538%26dopt%3DAbstract</link>
            <description>Authors: Pan-Hammarström Q, Zhao Y, Hammarström L
    Humans and mice separated more than 60 million years ago. Since then, evolution has led to a multitude of changes in their genomic sequences. The divergence of genes has resulted in differences both in the innate and adaptive immune systems. In this chapter, we focus on species difference with regard to immunoglobulin class switch recombination (CSR). We have compared the immunoglobulin constant region gene loci from human and mouse, with an emphasis on the switch regions, germ line transcription promoters, and 3' enhancers. We have also compared pathways/factors that are involved in CSR. Although there are remarkable similarities in the cellular machinery involved in CSR, there are also a number of unique features in each species.
  ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=504196</comments>
            <pubDate>Tue, 27 Mar 2007 22:32:02 +0100</pubDate>
            <guid isPermaLink="false">504196</guid>        </item>
        <item>
            <title>Anti-IgE Antibodies for the Treatment of IgE-Mediated Allergic Diseases.</title>
            <link>http://www.medworm.com/index.php?rid=504195&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17383539%26dopt%3DAbstract</link>
            <description>Authors: Chang TW, Wu PC, Hsu CL, Hung AF
    The pharmacological purposes of the anti-IgE therapy are to neutralize IgE and to inhibit its production to attenuate type I hypersensitivity reactions. The therapy is based on humanized IgG1antibodies that bind to free IgE and to membrane-bound IgE on B cells, but not to IgE bound by the high-affinity IgE.Fc receptors on basophils and mast cells or by the low-affinity IgE.Fc receptors on B cells. After nearly 20 years since inception, therapeutic anti-IgE antibodies (anti-IgE) have been studied in about 30 Phase II and III clinical trials in many allergy indications, and a lead antibody, omalizumab, has been approved for treating patients (12 years and older) with moderate-to-severe allergic asthma. Anti-IgE has confirmed the roles of IgE in t...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=504195</comments>
            <pubDate>Tue, 27 Mar 2007 22:32:02 +0100</pubDate>
            <guid isPermaLink="false">504195</guid>        </item>
        <item>
            <title>Immune semaphorins: increasing members and their diverse roles.</title>
            <link>http://www.medworm.com/index.php?rid=504194&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17383540%26dopt%3DAbstract</link>
            <description>Authors: Kikutani H, Suzuki K, Kumanogoh A
    The semaphorin family consists of soluble and membrane-bound proteins originally identified as axonal guidance cues functioning during neuronal development. However, it is becoming increasingly clear that semaphorins play diverse roles in organogenesis, vascular growth, and tumor progression. In addition, emerging evidence indicates that several semaphorins, called &quot;immune semaphorins,&quot; play crucial roles also during immune responses. Extensive studies on the immune semaphorins have revealed not only parallels but also differences in the semaphorin functions between the immune and nervous systems, providing unexpected but meaningful insights into the biological activities of these molecules. This chapter focuses on our current understanding of...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=504194</comments>
            <pubDate>Tue, 27 Mar 2007 22:32:02 +0100</pubDate>
            <guid isPermaLink="false">504194</guid>        </item>
        <item>
            <title>Tec kinases in T cell and mast cell signaling.</title>
            <link>http://www.medworm.com/index.php?rid=504193&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17383541%26dopt%3DAbstract</link>
            <description>Authors: Felices M, Falk M, Kosaka Y, Berg LJ
    The Tec family of tyrosine kinases consists of five members (Itk, Rlk, Tec, Btk, and Bmx) that are expressed predominantly in hematopoietic cells. The exceptions, Tec and Bmx, are also found in endothelial cells. Tec kinases constitute the second largest family of cytoplasmic protein tyrosine kinases. While B cells express Btk and Tec, and T cells express Itk, Rlk, and Tec, all four of these kinases (Btk, Itk, Rlk, and Tec) can be detected in mast cells. This chapter will focus on the biochemical and cell biological data that have been accumulated regarding Itk, Rlk, Btk, and Tec. In particular, distinctions between the different Tec kinase family members will be highlighted, with a goal of providing insight into the unique functions of eac...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=504193</comments>
            <pubDate>Tue, 27 Mar 2007 22:32:02 +0100</pubDate>
            <guid isPermaLink="false">504193</guid>        </item>
        <item>
            <title>Integrin regulation of lymphocyte trafficking: lessons from structural and signaling studies.</title>
            <link>http://www.medworm.com/index.php?rid=504192&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17383542%26dopt%3DAbstract</link>
            <description>Authors: Kinashi T
    High trafficking capability of lymphocytes is crucial in immune surveillance and antigen responses. Central to this regulatory process is a dynamic control of lymphocyte adhesion behavior regulated by chemokines and adhesion receptors such as integrins. Modulation of lymphocyte adhesive responses occurs in a wide range of time window from less than a second to hours, enabling rolling lymphocyte to attach to and migrate through endothelium and interact with antigen-presenting cells. While there has been a rapid progress in the understanding of integrin structure, elucidation of signaling events to relay extracellular signaling to integrins in physiological contexts has recently emerged from studies using gene-targeting and gene-silencing technique. Regulatory molecule...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=504192</comments>
            <pubDate>Tue, 27 Mar 2007 22:32:02 +0100</pubDate>
            <guid isPermaLink="false">504192</guid>        </item>
        <item>
            <title>Regulation of immune responses and hematopoiesis by the rap1 signal.</title>
            <link>http://www.medworm.com/index.php?rid=504191&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17383543%26dopt%3DAbstract</link>
            <description>Authors: Minato N, Kometani K, Hattori M
    Rap1 (Ras-proximity 1), a member of the Ras family of small guanine triphosphatases (GTPases), is activated by diverse extracellular stimuli. While Rap1 has been discovered originally as a potential Ras antagonist, accumulating evidence indicates that Rap1 per se mediates unique signals and exerts biological functions distinctly different from Ras. Rap1 plays a dominant role in the control of cell-cell and cell-matrix interactions by regulating the function of integrins and other adhesion molecules in various cell types. Rap1 also regulates MAP kinase (MAPK) activity in a manner highly dependent on the context of cell types. Recent studies (including gene-targeting analysis) have uncovered that the Rap1 signal is integrated crucially and unpredi...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=504191</comments>
            <pubDate>Tue, 27 Mar 2007 22:32:02 +0100</pubDate>
            <guid isPermaLink="false">504191</guid>        </item>
        <item>
            <title>Lung dendritic cell migration.</title>
            <link>http://www.medworm.com/index.php?rid=504189&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17383544%26dopt%3DAbstract</link>
            <description>Authors: Hammad H, Lambrecht BN
    Dendritic cells (DCs) are crucial in regulating the immune response by bridging innate and adaptive immunity. DCs are constantly migrating from the blood to the lungs and from the lungs to the draining lymph nodes. How DCs populate the lung in the absence of inflammation and how they are recruited there during inflammation remain unclear. Since DCs play a central role in immune responses, both under steady-state and inflammatory conditions, detailed characterization of their migratory behavior may be essential for the development of future therapeutic strategies.
    PMID: 17383544 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=504189</comments>
            <pubDate>Tue, 27 Mar 2007 22:32:02 +0100</pubDate>
            <guid isPermaLink="false">504189</guid>        </item>
        <item>
            <title>Posttranscriptional mechanisms regulating the inflammatory response.</title>
            <link>http://www.medworm.com/index.php?rid=392819&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682271%26dopt%3DAbstract</link>
            <description>Authors: Stoecklin G, Anderson P
    The inflammatory response is a complex physiologic process that requires the coordinate induction of cytokines, chemokines, angiogenic factors, effector-enzymes, and proteases. Although transcriptional activation is required to turn on the inflammatory response, recent studies have revealed that posttranscriptional mechanisms play an important role by determining the rate at which mRNAs encoding inflammatory effector proteins are translated and degraded. Most posttranscriptional control mechanisms function to dampen the expression of pro-inflammatory proteins to ensure that potentially injurious proteins are not overexpressed during an inflammatory response. Here we discuss the factors that regulate the stability and translation of mRNAs encoding pro-in...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392819</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392819</guid>        </item>
        <item>
            <title>Negative signaling in Fc receptor complexes.</title>
            <link>http://www.medworm.com/index.php?rid=392816&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682272%26dopt%3DAbstract</link>
            <description>Authors: Daëron M, Lesourne R
    Cell activation results from the transient displacement of an active balance between positive and negative signaling. This displacement depends in part on the engagement of cell surface receptors by extracellular ligands. Among these are receptors for the Fc portion of immunoglobulins (FcRs). FcRs are widely expressed by cells of hematopoietic origin. When binding antibodies, FcRs provide these cells with immunoreceptors capable of triggering numerous biological responses in response to a specific antigen. FcR-dependent cell activation is regulated by negative signals which are generated together with positive signals within signalosomes that form upon FcR engagement. Many molecules involved in positive signaling, including the FcRbeta subunit, the src ki...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392816</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392816</guid>        </item>
        <item>
            <title>The surprising diversity of lipid antigens for CD1-restricted T cells.</title>
            <link>http://www.medworm.com/index.php?rid=392813&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682273%26dopt%3DAbstract</link>
            <description>Authors: Moody DB
    CD1 proteins have been conserved throughout mammalian evolution and function to present lipid antigens to T cells. Crystal structures of CD1-lipid complexes show that CD1 antigen-binding grooves are composed of four pockets and two antigen entry portals. This structural information now provides a detailed understanding of how CD1-binding grooves capture a surprisingly diverse array of lipid ligands. CD1-expressing APCs are able to acquire lipid antigens from their own pool of lipids and from exogenous sources, including microbial pathogens, bystander cells, or even the systemic circulation. CD1 proteins bind to certain antigens using high stringency loading reactions within endosomes that involve low pH, glycosidases, and lipid transfer proteins. Other antigens can di...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392813</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392813</guid>        </item>
        <item>
            <title>Lysophospholipids as mediators of immunity.</title>
            <link>http://www.medworm.com/index.php?rid=392810&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682274%26dopt%3DAbstract</link>
            <description>Authors: Lin DA, Boyce JA
    Lysophospholipids (LPLs) are lipid-derived signaling molecules exemplified by lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P). Originally identified as serum-associated growth factors, these mediators now are known to signal through a family of diverse G protein-coupled receptors (GPCRs). Virtually all cells that participate in the immune response express multiple receptors for LPLs. The development of antibody reagents that recognize the receptors for each LPL and the derivation of receptor-selective agonists and receptor-null mouse strains have provided insights into the widely diverse functions of LPLs in immune responses, particularly the role of S1P in lymphocyte trafficking. This review focuses on the biology of the LPLs as these molecules ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392810</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392810</guid>        </item>
        <item>
            <title>Systemic mastocytosis.</title>
            <link>http://www.medworm.com/index.php?rid=392807&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682275%26dopt%3DAbstract</link>
            <description>Authors: Robyn J, Metcalfe DD
    Systemic mastocytosis is a fascinating disease with diverse clinical features. There have been numerous advances in understanding the basis of clinical manifestations of this disease and of its molecular pathogenesis in the last several decades. The development of methods to study mast cell biology using cell culture and murine models has proven invaluable in this regard. Clarification of the roles of mast cells in various biological processes has expanded our understanding of their importance in innate immunity, as well as allergy. New diagnostic methods have allowed the design of detailed criteria to assist in distinguishing reactive mast cell hyperplasia from systemic mastocytosis. Variants and subvariants of systemic mastocytosis have been defined to a...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392807</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392807</guid>        </item>
        <item>
            <title>Regulation of fibrosis by the immune system.</title>
            <link>http://www.medworm.com/index.php?rid=392804&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682276%26dopt%3DAbstract</link>
            <description>Authors: Lupher ML, Gallatin WM
    Inflammation and fibrosis are two inter-related conditions with many overlapping mechanisms. Three specific cell types, macrophages, T helper cells, and myofibroblasts, each play important roles in regulating both processes. Following tissue injury, an inflammatory stimulus is often necessary to initiate tissue repair, where cytokines released from resident and infiltrating leukocytes stimulate proliferation and activation of myofibroblasts. However, in many cases this drive stimulates an inappropriate pro-fibrotic response. In addition, activated myofibroblasts can take on the role of traditional APCs, secrete pro-inflammatory cytokines, and recruit inflammatory cells to fibrotic foci, amplifying the fibrotic response in a vicious cycle. Moreover, infla...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392804</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392804</guid>        </item>
        <item>
            <title>Immunity and acquired alterations in cognition and emotion: lessons from SLE.</title>
            <link>http://www.medworm.com/index.php?rid=392801&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682277%26dopt%3DAbstract</link>
            <description>Authors: Diamond B, Kowal C, Huerta PT, Aranow C, Mackay M, DeGiorgio LA, Lee J, Triantafyllopoulou A, Cohen-Solal J, Volpe BT
    Classic immunologic teaching describes the brain as an immunologically privileged site. Studies of neuroimmunology have focused for many years almost exclusively on multiple sclerosis, a disease in which inflammatory cells actually infiltrate brain tissue, and the rodent model of this disease, experimental allergic encephalitis. Over the past decade, however, increasingly, brain-reactive antibodies have been demonstrated in the serum of patients with numerous neurological diseases. The contribution these antibodies make to neuronal dysfunction has, in general, not been determined. Here, we describe recent studies showing that serum antibodies to the N-methyl-D-...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392801</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392801</guid>        </item>
        <item>
            <title>Immunodeficiencies with autoimmune consequences.</title>
            <link>http://www.medworm.com/index.php?rid=392798&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16682278%26dopt%3DAbstract</link>
            <description>Authors: Notarangelo LD, Gambineri E, Badolato R
    Far from being mutually exclusive, immunodeficiency and autoimmunity may occur simultaneously. During the last years, analysis of Autoimmune Polyendocrinopathy--Candidiasis--Ectodermal Dystrophy (APECED) and Immunodysregulation--Polyendocrinopathy--Enteropathy--X-linked (IPEX), two rare monogenic forms of immunodeficiency associated with autoimmunity, has led to the identification of Auto Immune Regulator (AIRE) and Forkhead Box P3 (FOXP3), essential transcriptional regulators, involved in central tolerance and peripheral immune homeostasis, respectively. Characterization of the molecular and cellular mechanisms involved in APECED, and recognition that AIRE expression is sustained by effective thymopoiesis, has recently allowed to define...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392798</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392798</guid>        </item>
        <item>
            <title>Preface.</title>
            <link>http://www.medworm.com/index.php?rid=392794&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730259%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 16730259 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392794</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392794</guid>        </item>
        <item>
            <title>Cancer immunosurveillance and immunoediting: the roles of immunity in suppressing tumor development and shaping tumor immunogenicity.</title>
            <link>http://www.medworm.com/index.php?rid=392791&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730260%26dopt%3DAbstract</link>
            <description>Authors: Smyth MJ, Dunn GP, Schreiber RD
    Cellular transformation and tumor development result from an accumulation of mutational and epigenetic changes that alter normal cell growth and survival pathways. For the last 100 years, there has been a vigorous debate as to whether the unmanipulated immune system can detect and eliminate such altered host derived cells despite the fact that cancer cells frequently express either abnormal proteins or abnormal levels of normal cellular proteins that function as tumor antigens. In this review, we discuss the current state of this argument and point out some of the recent key experiments demonstrating that immunity not only protects the host from cancer development (i.e., provides a cancer immunosurveillance function) but also can promote tumor g...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392791</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392791</guid>        </item>
        <item>
            <title>Mechanisms of immune evasion by tumors.</title>
            <link>http://www.medworm.com/index.php?rid=392788&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730261%26dopt%3DAbstract</link>
            <description>Authors: Drake CG, Jaffee E, Pardoll DM
    In the past decade, basic studies in animal models have begun to elucidate the physiological barriers which impede a successful antitumor immune response. These barriers operate at a number of levels, and involve the tumor, the tumor microenvironment and various components of the innate and adaptive immune systems. In this review, we discuss the multiple mechanisms by which tumors evade an immune response, with an emphasis on clinically relevant strategies to overcome these inhibitory checkpoints.
    PMID: 16730261 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392788</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392788</guid>        </item>
        <item>
            <title>Development of antibodies and chimeric molecules for cancer immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=392785&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730262%26dopt%3DAbstract</link>
            <description>Authors: Waldmann TA, Morris JC
    Monoclonal antibodies are among the most rapidly expanding class of therapeutics for cancer treatment. Monoclonal antibodies targeting non-Hodgkin's lymphoma (NHL), Her-2/neu highly expressing metastatic breast cancer, colorectal cancer, acute myelogenous leukemia, and B-cell chronic lymphocytic leukemia (CLL) have received FDA approval. Promising new targets for antibody therapy include cellular growth factor receptors, mediators of tumor-driven neo-angiogenesis, as well as host negative immunoregulatory checkpoints that impede an effective immune response to neoplasia. Antibody efficacy has been increased by genetic engineering to humanize the antibodies and to increase their effector functions including antibody dependent cellular cytotoxicity. Furthe...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392785</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392785</guid>        </item>
        <item>
            <title>Induction of tumor immunity following allogeneic stem cell transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=392782&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730263%26dopt%3DAbstract</link>
            <description>Authors: Wu CJ, Ritz J
    The curative potential of allogeneic hematopoietic stem cell transplantation (allo-HSCT) for many hematologic malignancies derives in large part from reconstitution of normal donor immunity and the development of a potent graft-versus-leukemia (GVL) immune response capable of rejecting tumor cell in vivo. Elucidation of the mechanisms of GVL by studies of animal models and analysis of clinical data has yielded important insights into how clinically effective tumor immunity is generated following allo-HSCT. These studies have identified NK cells and B cells as well as T cells as important mediators of the GVL response. A variety of antigenic targets of the GVL response have also been identified, and include tumor-associated antigens as well as minor histocompatibi...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392782</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392782</guid>        </item>
        <item>
            <title>Vaccination for treatment and prevention of cancer in animal models.</title>
            <link>http://www.medworm.com/index.php?rid=392779&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730264%26dopt%3DAbstract</link>
            <description>Authors: Cavallo F, Offringa R, van der Burg SH, Forni G, Melief CJ
    Two approaches to immunological intervention in tumor-host interactions in mouse models are discussed in this review. The first is described with reference to experiments in which CD8(+) T lymphocytes are used to kill established transplantable tumors. Peptides and their optimal presentation by dendritic cells and intervention in immune regulatory mechanisms are the key issues for efficient induction of T-killer cell-mediated tumor eradication. The time frame of tumor therapy and the threat imposed by tumor growth in transplantable models and cancer patients require the induction of a robust T-cell reaction. Prevention of the progression of small preneoplastic lesions, on the other hand, requires the significant and pr...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392779</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392779</guid>        </item>
        <item>
            <title>Unraveling the complex relationship between cancer immunity and autoimmunity: lessons from melanoma and vitiligo.</title>
            <link>http://www.medworm.com/index.php?rid=392776&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730265%26dopt%3DAbstract</link>
            <description>Authors: Uchi H, Stan R, Turk MJ, Engelhorn ME, Rizzuto GA, Goldberg SM, Wolchok JD, Houghton AN
    A relationship between melanoma and vitiligo, a skin disorder characterized by the loss of melanocytes, has been postulated for many decades. In some cases, vitiligo is almost certainly a manifestation of autoimmune-mediated destruction of melanocytes. Melanocytes and melanoma cells share melanocyte differentiation antigens. Based on a number of observations, de novo vitiligo developing in patients with melanoma has been regarded as a sign of good prognosis. The immune system tolerates or ignores differentiation antigens because these antigens are self-derived. Therefore, immune tolerance or ignorance must be overcome to prime naive T and B cells to induce cancer immunity and autoimmunity a...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392776</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392776</guid>        </item>
        <item>
            <title>Immunity to melanoma antigens: from self-tolerance to immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=392773&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730266%26dopt%3DAbstract</link>
            <description>Authors: Slingluff CL, Chianese-Bullock KA, Bullock TN, Grosh WW, Mullins DW, Nichols L, Olson W, Petroni G, Smolkin M, Engelhard VH
    The development of effective immune therapy for cancer is a central goal of immunologists in the 21st century. Our laboratories have been deeply involved in characterization of the immune response to melanoma and translation of laboratory discoveries into clinical trials. We have identified a cohort of peptide antigens presented by Major Histocompatibility Complex (MHC) molecules on melanoma cells and widely recognized by T cells from melanoma patients. These have been incorporated into peptide-based vaccines that induce CD8(+) and CD4(+) T-cell responses in 80-100% of patients. Major objective clinical tumor regressions have been observed in some patient...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392773</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392773</guid>        </item>
        <item>
            <title>Checkpoint blockade in cancer immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=392770&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730267%26dopt%3DAbstract</link>
            <description>Authors: Korman AJ, Peggs KS, Allison JP
    The progression of a productive immune response requires that a number of immunological checkpoints be passed. Passage may require the presence of excitatory costimulatory signals or the avoidance of negative or coinhibitory signals, which act to dampen or terminate immune activity. The immunoglobulin superfamily occupies a central importance in this coordination of immune responses, and the CD28/cytotoxic T-lymphocyte antigen-4 (CTLA-4):B7.1/B7.2 receptor/ligand grouping represents the archetypal example of these immune regulators. In part the role of these checkpoints is to guard against the possibility of unwanted and harmful self-directed activities. While this is a necessary function, aiding in the prevention of autoimmunity, it may act as ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392770</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392770</guid>        </item>
        <item>
            <title>Combinatorial cancer immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=392767&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16730268%26dopt%3DAbstract</link>
            <description>Authors: Hodi FS, Dranoff G
    The formulation of therapeutic strategies to enhance immune-mediated tumor destruction is a central goal of cancer immunology. Substantive progress toward delineating the mechanisms involved in innate and adaptive tumor immunity has improved the prospects for crafting efficacious treatments. Schemes under active clinical evaluation include cancer vaccines, monoclonal antibodies, recombinant cytokines, and adoptive cellular infusions. While these manipulations increase tumor immunity in many patients, the majority still succumbs to progressive disease. Detailed analysis of subjects on experimental protocols together with informative studies of murine tumor models have begun to clarify the parameters that determine therapeutic activity and resistance. These in...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392767</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392767</guid>        </item>
        <item>
            <title>A reappraisal of humoral immunity based on mechanisms of antibody-mediated protection against intracellular pathogens.</title>
            <link>http://www.medworm.com/index.php?rid=392764&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16938537%26dopt%3DAbstract</link>
            <description>Authors: Casadevall A, Pirofski LA
    Sometime in the mid to late twentieth century the study of antibody-mediated immunity (AMI) entered the doldrums, as many immunologists believed that the function of AMI was well understood, and was no longer deserving of intensive investigation. However, beginning in the 1990s studies using monoclonal antibodies (mAbs) revealed new functions for antibodies, including direct antimicrobial effects and their ability to modify host inflammatory and cellular responses. Furthermore, the demonstration that mAbs to several intracellular bacterial and fungal pathogens were protective issued a serious challenge to the paradigm that host defense against such microbes was strictly governed by cell-mediated immunity (CMI). Hence, a new view of AMI is emerging. Th...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392764</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392764</guid>        </item>
        <item>
            <title>Accessibility control of V(D)J recombination.</title>
            <link>http://www.medworm.com/index.php?rid=392759&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16938538%26dopt%3DAbstract</link>
            <description>Authors: Cobb RM, Oestreich KJ, Osipovich OA, Oltz EM
    Mammals contend with a universe of evolving pathogens by generating an enormous diversity of antigen receptors during lymphocyte development. Precursor B and T cells assemble functional immunoglobulin (Ig) and T cell receptor (TCR) genes via recombination of numerous variable (V), diversity (D), and joining (J) gene segments. Although this combinatorial process generates significant diversity, genetic reorganization is inherently dangerous. Thus, V(D)J recombination must be tightly regulated to ensure proper lymphocyte development and avoid chromosomal translocations that cause lymphoid tumors. Each genomic rearrangement is mediated by a common V(D)J recombinase that recognizes sequences flanking all antigen receptor gene segments. ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392759</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392759</guid>        </item>
        <item>
            <title>Targeting integrin structure and function in disease.</title>
            <link>http://www.medworm.com/index.php?rid=392753&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16938539%26dopt%3DAbstract</link>
            <description>Authors: Staunton DE, Lupher ML, Liddington R, Gallatin WM
    Initially linked to the pathogenesis of inflammatory and hematologic diseases, integrins have become validated drug targets with the approval of five drugs. Moreover, there are several promising drug candidates in preclinical and clinical stages of development for multiple clinical indications. Integrins are attractive drug targets as their antagonism can block several steps in disease progression or maintenance. Integrin inhibitors can block the proliferation, migration, or tissue localization of inflammatory, angiogenic, and tumor cells, as well as signaling and gene expression contributing to disease. There has been a rapid increase in the elucidation of integrin structure, their allosteric mechanisms of bidirectional signal...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392753</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392753</guid>        </item>
        <item>
            <title>Endogenous TLR ligands and autoimmunity.</title>
            <link>http://www.medworm.com/index.php?rid=392747&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16938540%26dopt%3DAbstract</link>
            <description>Authors: Wagner H
    Based on an evolutionary conserved repertoire Toll-like-receptors (TLRs) donate specificity to innate immune cells. Therefore, TLRs are considered as paradigmatic for &quot;self&quot; versus &quot;non-self&quot; discrimination. This view, however, needs to be modified since TLR's also appear to recognise &quot;endogeneous&quot;, that is host-derived ligands, examples being host-derived DNA and -RNA. Here I discuss physiological and pathophysiological consequences of endogeneous ligand-recognition by TLRs. I conclude that endogeneous ligand recognition by TLRs drives sterile inflammation sustained by innate immune cells in certain autoimmune disorders.
    PMID: 16938540 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392747</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392747</guid>        </item>
        <item>
            <title>Genetic analysis of innate immunity.</title>
            <link>http://www.medworm.com/index.php?rid=392742&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16938541%26dopt%3DAbstract</link>
            <description>Authors: Hoebe K, Jiang Z, Tabeta K, Du X, Georgel P, Crozat K, Beutler B
    The inflammatory response to microbes--and host perception of microbes in general--is largely initiated by a single class of receptors, named for their similarity to the prototypic Toll receptor of Drosophila. The mammalian Toll-like receptors (TLRs) are ultimately responsible for most phenomena associated with infection. This includes both &quot;good&quot; effects of infection (e.g., the induction of lasting specific immunity to an infectious agent) and &quot;bad&quot; effects of infection (systemic inflammation and shock). Although they are essential for host defense, no other endogenous proteins can match their lethal potential. The TLR complexes transduce the toxicity of lipopolysaccharide (LPS), cysteinyl lipopeptides, and many...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392742</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392742</guid>        </item>
        <item>
            <title>TIM family of genes in immunity and tolerance.</title>
            <link>http://www.medworm.com/index.php?rid=392738&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16938542%26dopt%3DAbstract</link>
            <description>Authors: Kuchroo VK, Meyers JH, Umetsu DT, DeKruyff RH
    T cells on activation differentiate into different subsets (Th1 or Th2) with distinct effector functions. These T cell subsets are primarily differentiated on the basis of the cytokines that they produce, however, we have identified a novel gene family called TIM (T cell, immunoglobulin, mucin domain-containing molecules), whose members are differentially expressed on Th1 and Th2 cells. Three of the family members (Tim-1, Tim-3, and Tim-4) are conserved between mouse and man. Genomic association of the TIM family and polymorphisms in both Tim-1 and Tim-3 in different immune-mediated diseases suggest that the family may have an important role in regulating immunity, both in terms of normal immune responses and in diseases like autoi...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392738</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392738</guid>        </item>
        <item>
            <title>Inhibition of inflammatory responses by leukocyte Ig-like receptors.</title>
            <link>http://www.medworm.com/index.php?rid=392734&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16938543%26dopt%3DAbstract</link>
            <description>Authors: Katz HR
    The immune system must effectively regulate the balance between beneficial and detrimental inflammation. This process is achieved in part through cell surface receptors that rapidly integrate activating and inhibitory signals. The inhibitory members of the leukocyte Ig-like receptor (LILR) family, termed LILRBs, are broadly distributed among cell populations in the immune system and potently counterregulate cell activation induced by stimuli of innate and adaptive immune responses. Studies in mice and humans indicate that LILRBs appreciably downregulate harmful inflammatory responses induced by microbial, allergic, and cytotoxic mechanisms. Hence, the LILRBs likely play significant roles in regulating the incidence and severity of many inflammatory diseases, making the...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392734</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392734</guid>        </item>
        <item>
            <title>Systemic lupus erythematosus: multiple immunological phenotypes in a complex genetic disease.</title>
            <link>http://www.medworm.com/index.php?rid=392730&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17145301%26dopt%3DAbstract</link>
            <description>Authors: Fairhurst AM, Wandstrat AE, Wakeland EK
    Systemic lupus erythematosus (SLE) is a complex polygenic autoimmune disease characterized by the presence of anti-nuclear autoantibodies (ANAs) that are often detectable years prior to the onset of clinical disease. The disease is associated with a chronic activation of the immune system, with the most severe forms progressing to inflammatory damage that can impact multiple organ systems in afflicted individuals. Current therapeutic strategies poorly control disease manifestations and are generally immunosuppressive. Recent studies in human patient populations and animal models have associated elements of the innate immune system and abnormalities in the immature B lymphocyte receptor repertoires with disease initiation. A variety of cy...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392730</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392730</guid>        </item>
        <item>
            <title>Avian models with spontaneous autoimmune diseases.</title>
            <link>http://www.medworm.com/index.php?rid=392722&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17145302%26dopt%3DAbstract</link>
            <description>Authors: Wick G, Andersson L, Hala K, Gershwin ME, Selmi C, Erf GF, Lamont SJ, Sgonc R
    Autoimmune diseases in human patients only become clinically manifest when the disease process has developed to a stage where functional compensation by the afflicted organ or system is not possible anymore. In order to understand the initial etiologic and pathogenic events that are generally not yet accessible in humans, appropriate animal models are required. In this respect, spontaneously developing models--albeit rare--reflect the situation in humans much more closely than experimentally induced models, including knockout and transgenic mice. The present chapter describes three spontaneous chicken models for human autoimmune diseases, the Obese strain (OS) with a Hashimoto-like autoimmune thyroid...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392722</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392722</guid>        </item>
        <item>
            <title>Functional dynamics of naturally occurring regulatory T cells in health and autoimmunity.</title>
            <link>http://www.medworm.com/index.php?rid=392717&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17145303%26dopt%3DAbstract</link>
            <description>Authors: Levings MK, Allan S, d'Hennezel E, Piccirillo CA
    A network of regulatory T (Treg) cells exists to downregulate immune responses in various inflammatory circumstances and ultimately assure peripheral T cell tolerance. Naturally occurring CD4(+)CD25(+) Treg cell represents a major lymphocyte population engaged in the dominant control of self-reactive T responses and maintenance of tolerance within this network. CD4(+)CD25(+) Treg cells differentiate in the normal thymus as a functionally distinct subpopulation of T cells bearing a broad T cell receptor repertoire endowing these cells with the capacity to recognize a wide spectrum of self-Ag and non-self-Ag specificities. The development of CD4(+)CD25(+) Treg cells is genetically determined, influenced by Ag-specific and nonspeci...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392717</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392717</guid>        </item>
        <item>
            <title>BTLA and HVEM cross talk regulates inhibition and costimulation.</title>
            <link>http://www.medworm.com/index.php?rid=392711&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17145304%26dopt%3DAbstract</link>
            <description>Authors: Gavrieli M, Sedy J, Nelson CA, Murphy KM
    Recently a new inhibitory immunoglobulin domain-containing lymphocyte receptor was identified on the basis of its T helper 1 (T(H)1)-selective expression in murine T cell lines, which was named B and T lymphocyte attenuator (BTLA). Several groups have confirmed the initial characterization of BTLA as an inhibitory receptor, which was initially inferred from the mild increases in several parameters of BTLA-deficient mice. The initial expectation that BTLA would interact with a B7 family ligand, such as the B7x protein, was surprisingly overturned with the functional cloning of the actual BTLA ligand as herpesvirus entry mediator (HVEM). This was unexpected largely due to the fact that this interaction represents the convergence of two ve...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392711</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392711</guid>        </item>
        <item>
            <title>The human T cell response to melanoma antigens.</title>
            <link>http://www.medworm.com/index.php?rid=392707&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17145305%26dopt%3DAbstract</link>
            <description>Authors: Romero P, Cerottini JC, Speiser DE
    The cornerstone of the concept of immunosurveillance in cancer should be the experimental demonstration of immune responses able to alter the course of in vivo spontaneous tumor progression. Elegant genetic manipulation of the mouse immune system has proved this tenet. In parallel, progress in understanding human T cell mediated immunity has allowed to document the existence in cancer patients of naturally acquired T cell responses to molecularly defined tumor antigens. Various attributes of cutaneous melanoma tumors, notably their adaptability to in vitro tissue culture conditions, have contributed to convert this tumor in the prototype for studies of human antitumor immune responses. As a consequence, the first human cytolytic T lymphocyte ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392707</comments>
            <pubDate>Sun, 01 Jan 2006 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392707</guid>        </item>
        <item>
            <title>Adenosine deaminase deficiency: metabolic basis of immune deficiency and pulmonary inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=392888&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15705418%26dopt%3DAbstract</link>
            <description>Authors: Blackburn MR, Kellems RE
    Genetic deficiencies in the purine catabolic enzyme adenosine deaminase (ADA) in humans results primarily in a severe lymphopenia and immunodeficiency that can lead to the death of affected individuals early in life. The metabolic basis of the immunodeficiency is likely related to the sensitivity of lymphocytes to the accumulation of the ADA substrates adenosine and 2'-deoxyadenosine. Investigations using ADA-deficient mice have provided compelling evidence to support the hypothesis that T and B cells are sensitive to increased concentrations of 2'-deoxyadenosine that kill cells through mechanisms that involve the accumulation of dATP and the induction of apoptosis. In addition to effects on the developing immune system, ADA-deficient humans exhibit ph...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392888</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392888</guid>        </item>
        <item>
            <title>Mechanism and control of V(D)J recombination versus class switch recombination: similarities and differences.</title>
            <link>http://www.medworm.com/index.php?rid=392885&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15705419%26dopt%3DAbstract</link>
            <description>Authors: Dudley DD, Chaudhuri J, Bassing CH, Alt FW
    V(D)J recombination is the process by which the variable region exons encoding the antigen recognition sites of receptors expressed on B and T lymphocytes are generated during early development via somatic assembly of component gene segments. In response to antigen, somatic hypermutation (SHM) and class switch recombination (CSR) induce further modifications of immunoglobulin genes in B cells. CSR changes the IgH constant region for an alternate set that confers distinct antibody effector functions. SHM introduces mutations, at a high rate, into variable region exons, ultimately allowing affinity maturation. All of these genomic alteration processes require tight regulatory control mechanisms, both to ensure development of a normal im...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392885</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392885</guid>        </item>
        <item>
            <title>Isoforms of terminal deoxynucleotidyltransferase: developmental aspects and function.</title>
            <link>http://www.medworm.com/index.php?rid=392882&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15705420%26dopt%3DAbstract</link>
            <description>Authors: Thai TH, Kearney JF
    The immune system develops in a series of programmed developmental stages. Although recombination-activating gene (RAG) and nonhomologous end-joining (NHEJ) proteins are indispensable in the generation of immunoglobulins and T-cell receptors (TCRs), most CDR3 diversity is contributed by nontemplated addition of nucleotides catalyzed by the nuclear enzyme terminal deoxynucleotidyltransferase (TdT) and most nucleotide deletion is performed by exonucleases at V(D)J joins. Increasing TdT expression continuing into adult life results in N region addition and diversification of the T and B cell repertoires. In several species including mice and humans, there are multiple isoforms of TdT resulting from alternative mRNA splicing. The short form (TdTS) produces N ad...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392882</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392882</guid>        </item>
        <item>
            <title>Innate autoimmunity.</title>
            <link>http://www.medworm.com/index.php?rid=392879&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15705421%26dopt%3DAbstract</link>
            <description>Authors: Carroll MC, Holers VM
    The adaptive immune system has evolved highly specific pattern recognition proteins and receptors that, when triggered, provide a first line of host defense against pathogens. Studies reveal that these innate recognition proteins are also self-reactive and can initiate inflammation against self-tissues in a similar manner as with pathogens. This specific event is referred to as &quot;innate autoimmunity.&quot; In this review, we describe two classes of autoimmune responses, that is, reperfusion injury and fetal loss syndrome, in which the recognition and injury are mediated by innate immunity. Both disorders are common and are clinically important. Reperfusion injury (RI) represents an acute inflammatory response after a reversible ischemic event and subsequent res...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392879</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392879</guid>        </item>
        <item>
            <title>Formation of bradykinin: a major contributor to the innate inflammatory response.</title>
            <link>http://www.medworm.com/index.php?rid=392876&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15705422%26dopt%3DAbstract</link>
            <description>Authors: Joseph K, Kaplan AP
    The plasma kinin-forming cascade can be activated by contact with negatively charged macromolecules leading to binding and autoactivation of factor XII, activation of prekallikrein to kallikrein by factor XIIa, and cleavage of high molecular weight kininogen (HK) by kallikrein to release the vasoactive peptide bradykinin. Once kallikrein formation begins, there is rapid cleavage of unactivated factor XII to factor XIIa, and this positive feedback is favored kinetically over factor XII autoactivation. Examples of surface initiators that can function in this fashion are endotoxin, sulfated mucopolysaccharides, and aggregated Abeta protein. Physiological activation appears to occur along the surface of endothelial cells both by the aforementioned contact-initi...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392876</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392876</guid>        </item>
        <item>
            <title>Interleukin-2, interleukin-15, and their roles in human natural killer cells.</title>
            <link>http://www.medworm.com/index.php?rid=392873&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15705423%26dopt%3DAbstract</link>
            <description>Authors: Becknell B, Caligiuri MA
    Natural killer (NK) cells are CD56+CD3- large granular lymphocytes that constitute a key component of the human innate immune response. In addition to their potent cytolytic activity, NK cells elaborate a host of immunoregulatory cytokines and chemokines that play a crucial role in pathogen clearance. Furthermore, interactions between NK and other immune cells are implicated in triggering the adaptive, or antigen-specific, immune response. Interleukin-2 (IL-2) and IL-15 are two distinct cytokines with partially overlapping properties that are implicated in the development, homeostasis, and function of NK cells. This review examines the pervasive effects of IL-2 and IL-15 on NK cell biology, with an emphasis on recent discoveries and lingering challenge...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392873</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392873</guid>        </item>
        <item>
            <title>Regulation of antigen presentation and cross-presentation in the dendritic cell network: facts, hypothesis, and immunological implications.</title>
            <link>http://www.medworm.com/index.php?rid=392870&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15705424%26dopt%3DAbstract</link>
            <description>Authors: Wilson NS, Villadangos JA
    Dendritic cells (DCs) are central to the maintenance of immunological tolerance and the initiation and control of immunity. The antigen-presenting properties of DCs enable them to present a sample of self and foreign proteins, contained within an organism at any given time, to the T-cell repertoire. DCs achieve this communication with T cells by displaying antigenic peptides bound to MHC I and MHC II molecules. Here we review the studies carried out over the past 15 years to characterize these antigen presentation mechanisms, emphasizing their significance in relation to DC function in vivo. The life cycles of different DC populations found in vivo are described. Furthermore, we provide a critical assessment of the studies that examine the mechanisms ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392870</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392870</guid>        </item>
        <item>
            <title>Role of the LAT adaptor in T-cell development and Th2 differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=392867&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16102570%26dopt%3DAbstract</link>
            <description>Authors: Malissen B, Aguado E, Malissen M
    LAT (linker for activation of T cells) is an integral membrane adaptor protein that constitutes in T cells a major substrate of the ZAP-70 protein tyrosine kinase. LAT coordinates the assembly of a multiprotein signaling complex through phosphotyrosine-based motifs present within its intracytoplasmic segment. The resulting &quot;LAT signalosome&quot; links the TCR to the main intracellular signalling pathways that regulate T-cell development and T-cell function. Early studies using transformed T-cell lines suggested that LAT acts primarily as a positive regulator of T-cell receptor (TCR) signalling. The partial or complete inhibition of T-cell development observed in several mouse lines harboring mutant forms of LAT was congruent with that view. More rec...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392867</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392867</guid>        </item>
        <item>
            <title>The integration of conventional and unconventional T cells that characterizes cell-mediated responses.</title>
            <link>http://www.medworm.com/index.php?rid=392864&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16102571%26dopt%3DAbstract</link>
            <description>Authors: Pennington DJ, Vermijlen D, Wise EL, Clarke SL, Tigelaar RE, Hayday AC
    This review builds on evidence that cell-mediated immune responses to bacteria, viruses, parasites, and tumors are an integration of conventional and unconventional T-cell activities. Whereas conventional T cells provide clonal antigen-specific responses, unconventional T cells profoundly regulate conventional T cells, often suppressing their activities such that immunopathology is limited. By extrapolation, immunopathologies and inflammatory diseases may reflect defects in regulation by unconventional T cells. To explore the function of unconventional T cells, several extensive gene expression analyses have been undertaken. These studies are reviewed in some detail, with emphasis on the mechanisms by which...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392864</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392864</guid>        </item>
        <item>
            <title>Negative regulation of cytokine and TLR signalings by SOCS and others.</title>
            <link>http://www.medworm.com/index.php?rid=392861&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16102572%26dopt%3DAbstract</link>
            <description>Authors: Naka T, Fujimoto M, Tsutsui H, Yoshimura A
    
    PMID: 16102572 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392861</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392861</guid>        </item>
        <item>
            <title>Pathogenic T-cell clones in autoimmune diabetes: more lessons from the NOD mouse.</title>
            <link>http://www.medworm.com/index.php?rid=392858&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16102573%26dopt%3DAbstract</link>
            <description>Authors: Haskins K
    T-cell clones that can efficiently transfer diabetes to prediabetic nonobese diabetic (NOD) mice provide a powerful approach to dissecting the autoimmune disease process and for investigating immunoregulation. Diabetogenic T-cell clones carried in culture allow for detailed analysis of T-cell effector function and in vivo activity, and thus the contribution of a single clonotype to pathogenesis can be studied. As T cells comprising most or all of the repertoire in T-cell receptor transgenic (TCR-Tg) mice, diabetogenic T-cell clones have led to new variations on the NOD mouse model of autoimmune disease. T-cell clones are being used to screen peptide libraries and proteomic arrays to identify the autoantigens that drive these clones in vivo and to extend our knowledge...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392858</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392858</guid>        </item>
        <item>
            <title>The biology of human lymphoid malignancies revealed by gene expression profiling.</title>
            <link>http://www.medworm.com/index.php?rid=392855&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16102574%26dopt%3DAbstract</link>
            <description>Authors: Staudt LM, Dave S
    Gene expression profiling provides a quantitative molecular framework for the study of human lymphomas. This genomic technology has revealed that existing diagnostic categories are comprised of multiple molecularly and clinically distinct diseases. Diffuse large B-cell lymphoma (DLBCL), for example, consists of three gene expression subgroups, termed germinal center B-cell-like (GCB) DLBCL, activated B-cell-like (ABC) DLBCL, and primary mediastinal B-cell lymphoma (PMBL). These DLBCL subgroups arise from different stages of normal B-cell differentiation, utilize distinct oncogenic mechanisms, and differ in their ability to be cured by chemotherapy. Key regulatory factors and their target genes are differentially expressed among these subgroups, including BCL-...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392855</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392855</guid>        </item>
        <item>
            <title>New insights into alternative mechanisms of immune receptor diversification.</title>
            <link>http://www.medworm.com/index.php?rid=392852&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16102575%26dopt%3DAbstract</link>
            <description>Authors: Litman GW, Cannon JP, Rast JP
    The clonal commitment, selection, and expansion of B and T lymphocytes expressing diversified receptors provide the underlying basis for the jawed vertebrates adaptive immune response. At the core of this process is the rearrangement and somatic modification of segmental genetic elements that encode the constituent components of immunoglobulins and T-cell antigen receptors. No evidence has been found for a similar mechanism outside of jawed vertebrates; however, invertebrates and jawless vertebrates are subjected to continuous exposure to pathogenic bacteria, viruses, and parasites. The invertebrates and jawless vertebrates as well as jawed vertebrates all encode a variety of mediators of innate immunity. Several reports of extensive germline dive...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392852</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392852</guid>        </item>
        <item>
            <title>The repair of DNA damages/modifications during the maturation of the immune system: lessons from human primary immunodeficiency disorders and animal models.</title>
            <link>http://www.medworm.com/index.php?rid=392849&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16102576%26dopt%3DAbstract</link>
            <description>Authors: Revy P, Buck D, le Deist F, de Villartay JP
    The immune system is the site of various genotoxic stresses that occur during its maturation as well as during immune responses. These DNA lesions/modifications are primarily the consequences of specific physiological processes such as the V(D)J recombination, the immunoglobulin class switch recombination (CSR), and the generation of somatic hypermutations (SHMs) within Ig variable domains. The DNA lesions can be introduced either by specific factors (RAG1 and RAG2 in the case of V(D)J recombination and AID in the case of CSR and SHM) or during the various phases of cellular proliferation and cellular activation. All these DNA lesions are taken care of by the diverse DNA repair machineries of the cell. Several animal models as well a...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392849</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392849</guid>        </item>
        <item>
            <title>Antibody class switch recombination: roles for switch sequences and mismatch repair proteins.</title>
            <link>http://www.medworm.com/index.php?rid=392846&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16102577%26dopt%3DAbstract</link>
            <description>Authors: Min IM, Selsing E
    Mechanisms and targeting of antibody class switch DNA recombination are reviewed. Particular emphasis is on the roles for the DNA sequences comprising switch (S) regions, including the S-region tandem repeats, and on the roles of proteins that are involved in both DNA mismatch repair and in class switch recombination.
    PMID: 16102577 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392846</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392846</guid>        </item>
        <item>
            <title>CD22: A Multifunctional Receptor That Regulates B Lymphocyte Survival and Signal Transduction.</title>
            <link>http://www.medworm.com/index.php?rid=392843&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16227086%26dopt%3DAbstract</link>
            <description>Authors: Tedder TF, Poe JC, Haas KM
    Recent advances in the study of CD22 indicate a complex role for this transmembrane glycoprotein member of the immunoglobulin superfamily in the regulation of B lymphocyte survival and proliferation. CD22 has been previously recognized as a potential lectin-like adhesion molecule that binds alpha2,6-linked sialic acid-bearing ligands and as an important regulator of B-cell antigen receptor (BCR) signaling. However, genetic studies in mice reveal that some CD22 functions are regulated by ligand binding, whereas other functions are ligand-independent and may only require expression of an intact CD22 cytoplasmic domain at the B-cell surface. Until recently, most of the functional activity of CD22 has been widely attributed to CD22's ability to recruit p...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392843</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392843</guid>        </item>
        <item>
            <title>Tetramer Analysis of Human Autoreactive CD4-Positive T Cells.</title>
            <link>http://www.medworm.com/index.php?rid=392840&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16227087%26dopt%3DAbstract</link>
            <description>Authors: Nepom GT
    Self-reactivity is an intrinsic property of the human immune system. Autoreactive T cells derive directly from the developmental requirement for TCR engagement by self-antigens during lymphocyte maturation. The fundamental questions implicating these autoreactive cells in human autoimmunity then, are not &quot;Where do they come from?&quot;, but rather &quot;Why do they persist?&quot;, &quot;How do they become activated?&quot;, and &quot;How are they regulated or deleted?&quot;. New technologies, in which peptide-MHC (pMHC) ligands used for T-cell recognition are utilized as soluble fluorescent multimers, now permit the direct visualization of antigen-specific autoreactive T-lymphocytes. By using multimer technology to study self-reactive cells present in autoimmune patients and control individuals, a very ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392840</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392840</guid>        </item>
        <item>
            <title>Regulation of Phospholipase C-gamma2 Networks in B Lymphocytes.</title>
            <link>http://www.medworm.com/index.php?rid=392837&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16227088%26dopt%3DAbstract</link>
            <description>Authors: Hikida M, Kurosaki T
    The modulation of inositol-1,4,5-trisphosphate (IP(3)), a product of phospholipase C (PLC) activity, is one of a common signaling mechanism used in many biological systems. B lymphocytes also rely on IP(3) and subsequent calcium signaling to ensure appropriate developmental outcomes, as well as antigen-specific responses. In establishing the optimal intensity and duration of the PLC-gamma activity, an important role has emerged for adaptor molecules, which direct the appropriate subcellular localization of PLC-gamma and induce its conformational changes. Generated IP(3) binds to IP(3) receptors located on the endoplasmic reticulum (ER), which in turn is essential for triggering calcium release from the ER and subsequent entry of extracellular calcium by so...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392837</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392837</guid>        </item>
        <item>
            <title>Role of human mast cells and basophils in bronchial asthma.</title>
            <link>http://www.medworm.com/index.php?rid=392834&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16227089%26dopt%3DAbstract</link>
            <description>Authors: Marone G, Triggiani M, Genovese A, Paulis AD
    Mast cells and basophils are the only cells expressing the tetrameric (alphabetagamma(2)) structure of the high affinity receptor for IgE (FcvarepsilonRI) and synthesizing histamine in humans. Human FcvarepsilonRI(+) cells are conventionally considered primary effector cells of bronchial asthma. There is now compelling evidence that these cells differ immunologically, biochemically, and pharmacologically, which suggests that they might play distinct roles in the appearance and fluctuation of the asthma phenotype. Recent data have revealed the complexity of the involvement of human mast cells and basophils in asthma and have shed light on the control of recruitment and activation of these cells in different lung compartments. Prelimi...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392834</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392834</guid>        </item>
        <item>
            <title>A Novel Recognition System for MHC Class I Molecules Constituted by PIR.</title>
            <link>http://www.medworm.com/index.php?rid=392831&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16227090%26dopt%3DAbstract</link>
            <description>Authors: Takai T
    The paired immunoglobulin (Ig)-like receptors (PIRs) represent a typical receptor pair of the Ig-like receptor family in which various combinations of ligand-receptor interaction provide a positive and negative regulation of immune cells, thus enabling those cells to respond properly to extrinsic stimuli. Activating PIR-A and inhibitory PIR-B are expressed in a wide range of cells in the murine immune system, such as B cells, mast cells, macrophages, and dendritic cells, mostly in a pair-wise fashion. PIRs bind to MHC class I molecules expressed ubiquitously on hematopoietic as well as nonhematopoietic cells. The unbalanced binding of PIR-A and PIR-B to MHC class I molecules may lead to the perturbation of cell development, regulation, and function as observed in PIR-B...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392831</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392831</guid>        </item>
        <item>
            <title>Dendritic cell biology.</title>
            <link>http://www.medworm.com/index.php?rid=392828&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16227091%26dopt%3DAbstract</link>
            <description>Authors: Granucci F, Foti M, Ricciardi-Castagnoli P
    Dendritic cells (DCs) are a special type of leukocytes able to alert the immune system to the presence of infections. They play a central role in the initiation of both innate and adaptive immune responses. This particular DC feature is regulated by the activation of specific receptors at the cell surface called Toll-like receptors (TLRs) that bind a number of microbial products collectively referred to as microbial-associated molecular patterns (MAMP). TLRs initiate a cascade of events, which together define the process of DC maturation. This phenomenon allows DCs to progressively acquire varying specific functions. DC maturation depends on the nature of the perturbation and permits unique and efficient immune responses for each path...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392828</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392828</guid>        </item>
        <item>
            <title>The Murine Diabetogenic Class II Histocompatibility Molecule I-A(g7): Structural and Functional Properties and Specificity of Peptide Selection.</title>
            <link>http://www.medworm.com/index.php?rid=392825&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16227092%26dopt%3DAbstract</link>
            <description>Authors: Suri A, Unanue ER
    The onset of type 1 diabetes mellitus (T1DM) is directly linked to the expression of class II MHC molecules. The NOD mouse, which is an excellent animal model for the human disease, expresses the I-A(g7) molecule that shares many features with the human diabetogenic class II MHC alleles. In this review, the structural, biochemical, and biological properties of the I-A(g7) molecules and how they relate to onset of diabetes is discussed. In particular, the focus is on the unique properties of peptide selection by I-A(g7) that reveal the preferred binding motif of diabetogenic MHC molecules and its role in display of peptides derived from islet beta cells.
    PMID: 16227092 [PubMed - in process] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392825</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392825</guid>        </item>
        <item>
            <title>RNAi and RNA-Based Regulation of Immune System Function.</title>
            <link>http://www.medworm.com/index.php?rid=392822&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D16227093%26dopt%3DAbstract</link>
            <description>Authors: Chowdhury D, Novina CD
    Gene regulation by short RNAs is a ubiquitous and important mode of control. MicroRNAs are short, single-strand RNAs that bind with partial complementarity to the 3' untranslated region of several genes to silence their expression. This expanding class of endogenous short RNAs are evolutionarily conserved and participate in control of development and cell-specific gene function. Several of these microRNAs have been cloned uniquely from mammalian lymphocytes suggesting specialized roles in lymphocyte development and function. In addition, several genes linked to RNAi in lower eukaryotes have mammalian homologs with specialized roles in adaptive immunity. For example, in worms, the nonsense-mediated decay (NMD) and RNAi pathways appear to be intricately li...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392822</comments>
            <pubDate>Sat, 01 Jan 2005 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392822</guid>        </item>
        <item>
            <title>Transcriptional regulation in neutrophils: teaching old cells new tricks.</title>
            <link>http://www.medworm.com/index.php?rid=392929&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14975254%26dopt%3DAbstract</link>
            <description>Authors: McDonald PP
    
    PMID: 14975254 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392929</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392929</guid>        </item>
        <item>
            <title>Tumor vaccines.</title>
            <link>http://www.medworm.com/index.php?rid=392928&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14975255%26dopt%3DAbstract</link>
            <description>Authors: Stevenson FK, Rice J, Zhu D
    
    PMID: 14975255 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392928</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392928</guid>        </item>
        <item>
            <title>Immunotherapy of allergic disease.</title>
            <link>http://www.medworm.com/index.php?rid=392927&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14975256%26dopt%3DAbstract</link>
            <description>Authors: Valenta R, Ball T, Focke M, Linhart B, Mothes N, Niederberger V, Spitzauer S, Swoboda I, Vrtala S, Westritschnig K, Kraft D
    
    PMID: 14975256 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392927</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392927</guid>        </item>
        <item>
            <title>Interactions of immunoglobulins outside the antigen-combining site.</title>
            <link>http://www.medworm.com/index.php?rid=392926&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14975257%26dopt%3DAbstract</link>
            <description>Authors: Nezlin R, Ghetie V
    
    PMID: 14975257 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392926</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392926</guid>        </item>
        <item>
            <title>The role of antibodies in mouse models of rheumatoid arthritis, and relevance to human disease.</title>
            <link>http://www.medworm.com/index.php?rid=392925&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14975258%26dopt%3DAbstract</link>
            <description>Authors: Monach PA, Benoist C, Mathis D
    
    PMID: 14975258 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392925</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392925</guid>        </item>
        <item>
            <title>MUC1 immunobiology: from discovery to clinical applications.</title>
            <link>http://www.medworm.com/index.php?rid=392924&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14975259%26dopt%3DAbstract</link>
            <description>Authors: Vlad AM, Kettel JC, Alajez NM, Carlos CA, Finn OJ
    
    PMID: 14975259 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392924</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392924</guid>        </item>
        <item>
            <title>Human models of inherited immunoglobulin class switch recombination and somatic hypermutation defects (hyper-IgM syndromes).</title>
            <link>http://www.medworm.com/index.php?rid=392923&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14975260%26dopt%3DAbstract</link>
            <description>Authors: Durandy A, Revy P, Fischer A
    
    PMID: 14975260 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392923</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392923</guid>        </item>
        <item>
            <title>The biological role of the C1 inhibitor in regulation of vascular permeability and modulation of inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=392922&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14975261%26dopt%3DAbstract</link>
            <description>Authors: Davis AE, Cai S, Liu D
    
    PMID: 14975261 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392922</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392922</guid>        </item>
        <item>
            <title>Lineage commitment and developmental plasticity in early lymphoid progenitor subsets.</title>
            <link>http://www.medworm.com/index.php?rid=392921&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15135627%26dopt%3DAbstract</link>
            <description>Authors: Traver D, Akashi K
    
    PMID: 15135627 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392921</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392921</guid>        </item>
        <item>
            <title>The CD4/CD8 lineage choice: new insights into epigenetic regulation during T cell development.</title>
            <link>http://www.medworm.com/index.php?rid=392920&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15135628%26dopt%3DAbstract</link>
            <description>Authors: Taniuchi I, Ellmeier W, Littman DR
    
    PMID: 15135628 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392920</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392920</guid>        </item>
        <item>
            <title>CD4/CD8 coreceptors in thymocyte development, selection, and lineage commitment: analysis of the CD4/CD8 lineage decision.</title>
            <link>http://www.medworm.com/index.php?rid=392918&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15135629%26dopt%3DAbstract</link>
            <description>Authors: Singer A, Bosselut R
    
    PMID: 15135629 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392918</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
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        <item>
            <title>Development and function of T helper 1 cells.</title>
            <link>http://www.medworm.com/index.php?rid=392916&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15135630%26dopt%3DAbstract</link>
            <description>Authors: O'Garra A, Robinson D
    
    PMID: 15135630 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392916</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
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        <item>
            <title>Th2 cells: orchestrating barrier immunity.</title>
            <link>http://www.medworm.com/index.php?rid=392914&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15135631%26dopt%3DAbstract</link>
            <description>Authors: Stetson DB, Voehringer D, Grogan JL, Xu M, Reinhardt RL, Scheu S, Kelly BL, Locksley RM
    
    PMID: 15135631 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392914</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
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        <item>
            <title>Generation, maintenance, and function of memory T cells.</title>
            <link>http://www.medworm.com/index.php?rid=392912&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15135632%26dopt%3DAbstract</link>
            <description>Authors: Burkett PR, Koka R, Chien M, Boone DL, Ma A
    
    PMID: 15135632 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392912</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392912</guid>        </item>
        <item>
            <title>CD8+ effector cells.</title>
            <link>http://www.medworm.com/index.php?rid=392910&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15135633%26dopt%3DAbstract</link>
            <description>Authors: Henkart PA, Catalfamo M
    
    PMID: 15135633 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392910</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392910</guid>        </item>
        <item>
            <title>An integrated model of immunoregulation mediated by regulatory T cell subsets.</title>
            <link>http://www.medworm.com/index.php?rid=392908&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15135634%26dopt%3DAbstract</link>
            <description>Authors: Jiang H, Chess L
    
    PMID: 15135634 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392908</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392908</guid>        </item>
        <item>
            <title>Interactions between NK cells and B lymphocytes.</title>
            <link>http://www.medworm.com/index.php?rid=392906&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15246249%26dopt%3DAbstract</link>
            <description>Authors: Yuan D
    
    PMID: 15246249 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392906</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
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        <item>
            <title>Multitasking of helix-loop-helix proteins in lymphopoiesis.</title>
            <link>http://www.medworm.com/index.php?rid=392904&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15246250%26dopt%3DAbstract</link>
            <description>Authors: Sun XH
    
    PMID: 15246250 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392904</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392904</guid>        </item>
        <item>
            <title>Customized antigens for desensitizing allergic patients.</title>
            <link>http://www.medworm.com/index.php?rid=392902&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15246251%26dopt%3DAbstract</link>
            <description>Authors: Ferreira F, Wallner M, Thalhamer J
    
    PMID: 15246251 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392902</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392902</guid>        </item>
        <item>
            <title>Immune response against dying tumor cells.</title>
            <link>http://www.medworm.com/index.php?rid=392900&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15246252%26dopt%3DAbstract</link>
            <description>Authors: Zitvogel L, Casares N, Péquignot MO, Chaput N, Albert ML, Kroemer G
    
    PMID: 15246252 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392900</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392900</guid>        </item>
        <item>
            <title>HMGB1 in the immunology of sepsis (not septic shock) and arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=392898&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15246253%26dopt%3DAbstract</link>
            <description>Authors: Czura CJ, Yang H, Amella CA, Tracey KJ
    
    PMID: 15246253 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392898</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392898</guid>        </item>
        <item>
            <title>Selection of the T-cell repertoire: receptor-controlled checkpoints in T-cell development.</title>
            <link>http://www.medworm.com/index.php?rid=392896&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15246254%26dopt%3DAbstract</link>
            <description>Authors: von Boehmer H
    
    PMID: 15246254 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392896</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392896</guid>        </item>
        <item>
            <title>The pathogenesis of diabetes in the NOD mouse.</title>
            <link>http://www.medworm.com/index.php?rid=392894&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15246255%26dopt%3DAbstract</link>
            <description>Authors: Solomon M, Sarvetnick N
    
    PMID: 15246255 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392894</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392894</guid>        </item>
        <item>
            <title>Advances in Immunology cumulative subject index, volumes 66-82.</title>
            <link>http://www.medworm.com/index.php?rid=392891&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D15551494%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 15551494 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392891</comments>
            <pubDate>Thu, 01 Jan 2004 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392891</guid>        </item>
        <item>
            <title>Regulation of the immune response by the interaction of chemokines and proteases.</title>
            <link>http://www.medworm.com/index.php?rid=392941&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14711052%26dopt%3DAbstract</link>
            <description>Authors: Struyf S, Proost P, Van Damme J
    
    PMID: 14711052 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392941</comments>
            <pubDate>Wed, 01 Jan 2003 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392941</guid>        </item>
        <item>
            <title>Molecular mechanisms of host-pathogen interaction: entry and survival of mycobacteria in macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=392939&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14711053%26dopt%3DAbstract</link>
            <description>Authors: Gatfield J, Pieters J
    
    PMID: 14711053 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392939</comments>
            <pubDate>Wed, 01 Jan 2003 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392939</guid>        </item>
        <item>
            <title>B lymphoid neoplasms of mice: characteristics of naturally occurring and engineered diseases and relationships to human disorders.</title>
            <link>http://www.medworm.com/index.php?rid=392938&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14711054%26dopt%3DAbstract</link>
            <description>Authors: Morse HC, McCarty T, Qi CF, Torrey TA, Naghashfar Z, Chattopadhyay SK, Fredrickson TN, Hartley JW
    
    PMID: 14711054 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392938</comments>
            <pubDate>Wed, 01 Jan 2003 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392938</guid>        </item>
        <item>
            <title>Prions and the immune system: a journey through gut, spleen, and nerves.</title>
            <link>http://www.medworm.com/index.php?rid=392936&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14711055%26dopt%3DAbstract</link>
            <description>Authors: Aguzzi A
    For more than two decades it has been contended that prion infection does not elicit immune responses: transmissible spongiform encephalopathies do not go along with conspicuous inflammatory infiltrates, and antibodies to the prion protein are typically undetectable. Why is it, then, that prions accumulate in lymphoid organs, and that various states of immune deficiency prevent peripheral prion infection? This review revisits the current evidence of the involvement of the immune system in prion diseases, while attempting to trace the elaborate mechanisms by which peripherally administered prions invade the brain and ultimately cause damage. The investigation of these questions leads to unexpected detours, including the neurophysiology of lymphoid organs, and even the ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392936</comments>
            <pubDate>Wed, 01 Jan 2003 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392936</guid>        </item>
        <item>
            <title>Roles of the semaphorin family in immune regulation.</title>
            <link>http://www.medworm.com/index.php?rid=392935&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14711056%26dopt%3DAbstract</link>
            <description>Authors: Kumanogoh A, Kikutani H
    The immune system and the nervous system have distinct roles in maintaining physiological homeostasis. These independent systems, however, influence each other while sharing common resources, including the cytokines and members of the immunoglobulin superfamily. Semaphorins are one of these shared molecular families that are biologically active in both systems. Although semaphorins were originally identified as axon guidance factors functioning in the nervous system, recent studies have uncovered additional immunological functions. For example, ligand-receptor systems distinct from those characterized in the nervous system govern class IV semaphorin, CD100/Sema4D and Sema4A activity in immune responses. This review provides an overview of the currently ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392935</comments>
            <pubDate>Wed, 01 Jan 2003 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392935</guid>        </item>
        <item>
            <title>HLA-G molecules: from maternal-fetal tolerance to tissue acceptance.</title>
            <link>http://www.medworm.com/index.php?rid=392934&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14711057%26dopt%3DAbstract</link>
            <description>Authors: Carosella ED, Moreau P, Le Maoult J, Le Discorde M, Dausset J, Rouas-Freiss N
    Over the past few years, HLA-G, the non-classical HLA class I molecule, has been the center of investigations that have led to the description of its specific structural and functional properties. Although located in the HLA class I region of chromosome six, the HLA-G gene may be distinguished from other HLA class I genes by its low polymorphism and alternative splicing that generates seven HLA-G proteins, whose tissue-distribution is restricted to normal fetal and adult tissues that display a tolerogeneic function toward both innate and acquired immune cells. We review these points, with special emphasis on the role of HLA-G in human pathologies, such as cancer, viral infection, and inflammatory dis...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392934</comments>
            <pubDate>Wed, 01 Jan 2003 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392934</guid>        </item>
        <item>
            <title>The zebrafish as a model organism to study development of the immune system.</title>
            <link>http://www.medworm.com/index.php?rid=392932&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14711058%26dopt%3DAbstract</link>
            <description>Authors: Traver D, Herbomel P, Patton EE, Murphey RD, Yoder JA, Litman GW, Catic A, Amemiya CT, Zon LI, Trede NS
    
    PMID: 14711058 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392932</comments>
            <pubDate>Wed, 01 Jan 2003 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392932</guid>        </item>
        <item>
            <title>Control of autoimmunity by naturally arising regulatory CD4+ T cells.</title>
            <link>http://www.medworm.com/index.php?rid=392930&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D14711059%26dopt%3DAbstract</link>
            <description>Authors: Hori S, Takahashi T, Sakaguchi S
    Naturally acquired immunological self-tolerance is not entirely accounted for by clonal deletion, anergy, and ignorance. It is now well established that the T cell-repertoire of healthy individuals harbors self-reactive lymphocytes with a potential to cause autoimmune disease and these lymphocytes are under dominant control by a unique subpopulation of CD4+ T cells now called regulatory T cells. Efforts to delineate these Treg cells naturally present in normal individuals have revealed that they are enriched in the CD25+ CD4+ population. The identification of the CD25 molecule as a useful marker for naturally arising CD4+ regulatory T cells has made it possible to investigate many key aspects of their immunobiology, including their antigen spec...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392930</comments>
            <pubDate>Wed, 01 Jan 2003 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392930</guid>        </item>
        <item>
            <title>Protein degradation and the generation of MHC class I-presented peptides.</title>
            <link>http://www.medworm.com/index.php?rid=392951&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D12078479%26dopt%3DAbstract</link>
            <description>Authors: Rock KL, York IA, Saric T, Goldberg AL
    Over the past decade there has been considerable progress in understanding how MHC class I-presented peptides are generated. The emerging theme is that the immune system has not evolved its own specialized proteolytic mechanisms but instead utilizes the phylogenetically ancient catabolic pathways that continually turnover proteins in all cells. Three distinct proteolytic steps have now been defined in MHC class I antigen presentation. The first step is the degradation of proteins by the ubiquitin-proteasome pathway into oligopeptides that either are of the correct size for presentation or are extended on their amino-termini. In the second step, aminopeptidases trim N-extended precursors into peptides of the correct length to be presented ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392951</comments>
            <pubDate>Tue, 01 Jan 2002 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392951</guid>        </item>
        <item>
            <title>Cytokine memory of T helper lymphocytes.</title>
            <link>http://www.medworm.com/index.php?rid=392949&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D12078480%26dopt%3DAbstract</link>
            <description>Authors: Löhning M, Richter A, Radbruch A
    Memory is one of the key features of the adaptive immune system. Specific T and B lymphocytes are primed for a particular antigen and upon challenge with it will react faster than naive lymphocytes. They also memorize the expression of key effector molecules, in particular cytokines, which determine the type and scale of an immune reaction. While in primary activations differential expression of cytokine genes is dependent on antigen-receptor signaling and differentiation signals, in later activations the expression is triggered by antigen-receptor signaling and dependent on the cytokine memory. The molecular basis of the cytokine memory implies differential expression of transcription factors and epigenetic modifications of cytokine genes and...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392949</comments>
            <pubDate>Tue, 01 Jan 2002 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392949</guid>        </item>
        <item>
            <title>Ig gene hypermutation: a mechanism is due.</title>
            <link>http://www.medworm.com/index.php?rid=392948&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D12078481%26dopt%3DAbstract</link>
            <description>Authors: Weill JC, Bertocci B, Faili A, Aoufouchi S, Frey S, De Smet A, Storck S, Dahan A, Delbos F, Weller S, Flatter E, Reynaud CA
    
    PMID: 12078481 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392948</comments>
            <pubDate>Tue, 01 Jan 2002 07:00:00 +0100</pubDate>
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            <title>Generalization of single immunological experiences by idiotypically mediated clonal connections.</title>
            <link>http://www.medworm.com/index.php?rid=392946&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D12078482%26dopt%3DAbstract</link>
            <description>Authors: Lemke H, Lange H
    Clonal interactions of B cells by idiotope-specific mutual recognition of their antigen receptors with the participation of T cells were assumed to form a web of unknown density, referred to as the idiotypic network. Although these clonal connections were proposed to fulfill important internal regulatory functions, their biological significance, especially in relation to antigen-induced immune responses, remained a mystery. In view of this, we postulate that the basic function of the idiotypic internal connection between B and T cell antigen receptors is to transform antigen-induced cellular activations, by idiotypic crossreactivity, into the regulation of cell clones with different antigen specificities. This process leads not only to the suppression of major...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
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            <pubDate>Tue, 01 Jan 2002 07:00:00 +0100</pubDate>
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        <item>
            <title>The aging of the immune system.</title>
            <link>http://www.medworm.com/index.php?rid=392944&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D12078483%26dopt%3DAbstract</link>
            <description>Authors: Grubeck-Loebenstein B, Wick G
    
    PMID: 12078483 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392944</comments>
            <pubDate>Tue, 01 Jan 2002 07:00:00 +0100</pubDate>
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            <title>Proteolysis and antigen presentation by MHC class II molecules.</title>
            <link>http://www.medworm.com/index.php?rid=392942&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D12078484%26dopt%3DAbstract</link>
            <description>Authors: Bryant PW, Lennon-Duménil AM, Fiebiger E, Lagaudrière-Gesbert C, Ploegh HL
    
    PMID: 12078484 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392942</comments>
            <pubDate>Tue, 01 Jan 2002 07:00:00 +0100</pubDate>
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            <title>Chemokines in immunity.</title>
            <link>http://www.medworm.com/index.php?rid=392964&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D11432208%26dopt%3DAbstract</link>
            <description>Authors: Yoshie O, Imai T, Nomiyama H
    Chemokines are a superfamily of small, heparin-binding cytokines that induce directed migration of various types of leukocytes through interactions with a group of seven-transmembrane G protein-coupled receptors. At present, over 40 members have been identified in humans. Until a few years ago, chemokines were mainly known as potent attractants for leukocytes such as neutrophils and monocytes, and were thus mostly regarded as the mediators of acute and chronic inflammatory responses. They had highly complex ligand-receptor relationships and their genes were regularly mapped on chromosomes 4 and 17 in humans. Recently, novel chemokines have been identified in rapid succession, mostly through application of bioinformatics on expressed sequence tag da...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392964</comments>
            <pubDate>Mon, 01 Jan 2001 07:00:00 +0100</pubDate>
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            <title>Neutralizing antiviral antibody responses.</title>
            <link>http://www.medworm.com/index.php?rid=392963&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D11680006%26dopt%3DAbstract</link>
            <description>Authors: Zinkernagel RM, LaMarre A, Ciurea A, Hunziker L, Ochsenbein AF, McCoy KD, Fehr T, Bachmann MF, Kalinke U, Hengartner H
    
    PMID: 11680006 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392963</comments>
            <pubDate>Mon, 01 Jan 2001 07:00:00 +0100</pubDate>
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            <title>Xenotransplantation.</title>
            <link>http://www.medworm.com/index.php?rid=392961&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D11680007%26dopt%3DAbstract</link>
            <description>Authors: Sachs DH, Sykes M, Robson SC, Cooper DK
    
    PMID: 11680007 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392961</comments>
            <pubDate>Mon, 01 Jan 2001 07:00:00 +0100</pubDate>
            <guid isPermaLink="false">392961</guid>        </item>
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            <title>Regulation of antibacterial and antifungal innate immunity in fruitflies and humans.</title>
            <link>http://www.medworm.com/index.php?rid=392960&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D11680008%26dopt%3DAbstract</link>
            <description>Authors: Williams MJ
    Insects have been very successful in adapting to their environment, and the ability of the insect immune system to detect and elicit the appropriate response against various invading pathogens has helped in this success. Unlike the vertebrate immune system, which consists of both innate and adaptive components, insect immunity probably consists entirely of an innate immune response, as no evidence of an adaptive response has been found. The innate immune response is described as either a reaction against &quot;lack of self,&quot; or the interaction between host germline-encoded receptors and molecules unique to a particular class of invading organisms. Once the invading organism is recognized, the host immune response can be activated via signaling pathways that lead to the ...</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392960</comments>
            <pubDate>Mon, 01 Jan 2001 07:00:00 +0100</pubDate>
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            <title>Functional heavy-chain antibodies in Camelidae.</title>
            <link>http://www.medworm.com/index.php?rid=392959&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D11680009%26dopt%3DAbstract</link>
            <description>Authors: Nguyen VK, Desmyter A, Muyldermans S
    
    PMID: 11680009 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392959</comments>
            <pubDate>Mon, 01 Jan 2001 07:00:00 +0100</pubDate>
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            <title>Uterine natural killer cells in the pregnant uterus.</title>
            <link>http://www.medworm.com/index.php?rid=392957&amp;cid=s_34425_3_f&amp;fid=34425&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D11680010%26dopt%3DAbstract</link>
            <description>Authors: Liu CC, Young JD
    
    PMID: 11680010 [PubMed - indexed for MEDLINE] (Source: Advances in Immunology)</description>
            <author>Advances in Immunology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=392957</comments>
            <pubDate>Mon, 01 Jan 2001 07:00:00 +0100</pubDate>
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