| Description |
1 online resource (x, 360 pages) : illustrations |
| Series |
Current directions in autoimmunity ; vol. 4 |
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Current directions in autoimmunity ; vol. 4.
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| Contents |
Preface -- Genetics of Human Type 3 Diabetes mellitus -- Genes and Cellular Requirements for Autoimmune Diabetes Susceptibility in Nonobese Diabetic Mice -- The Mucosal Interface between 'Self' and 'Non-Self' Determines the Impact of Environment on Autoimmune Diabetes -- Is Activation of Autoreactive Lymphocytes Always Detrimental? Viral Infections and Regulatory Circuits in Autoimmunity -- Defects in Deletional Tolerance of CD8 T Cells in Autoimmune Diabetes -- How Beta Cells Die in Type 3 Diabetes |
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Interactions of Effectors and Regulators Are Decisive in the Manifestations of Type 3 Diabetes in Nonobese Diabetic Mice -- Cytokine Regulation of Diabetes in Experimental Models -- Understanding the Interaction of Genetics and Cellular Responses in Nonobese Diabetic Mice -- Human T-Cell Responses to Islet Cell Antigens -- Autoantibodies in Human Diabetes -- Transplantation Tolerance -- Role of Regulatory T Cells in the Pathogenesis of Autoimmune Diabetes -- Immunotherapy of Type 3 Diabetes mellitus -- Author Index -- Subject Index |
| Summary |
Type 1 diabetes as well as multiple sclerosis are thought to be T cell mediated autoimmune diseases that involve a detrimental action of inflammatory cytokines and autoaggressive T lymphocytes. They still pose many unsolved puzzles, and the precise etiology as well as prevention have remained elusive. It is clear that genetic factors can predispose for developing diabetes, however, based on significant disease discordance found in monozygotic twins, additional environmental factors have to be postulated. Viruses are good candidates because they induce strong cellular and humoral immune responses, but no single etiologic agent has been identified. Several animal models are presented which have been used to study the activation of naive autoreactive lymphocytes. It is shown that regulation of the autoaggressive process occurs prior to clinical diabetes and is mediated by a complete network of cytokines, as well as regulatory circuits/cells. The spreading of autoimmunity to self-antigens not involved in the initial phase of islet destruction is not necessarily detrimental and can carry benefits. Therapeutically, counter-regulation of aggressive responses has been demonstrated via various means in animal models preventing diabetes or rejection of transplanted islets. All these findings are being discussed in this volume, which presents a state-of-the-art overview of the pathogenesis and intervention of type 1 diabetes. Authoritative and up-to-date, it will be of great value to any investigator interested in understanding autoimmunity |
| Bibliography |
Includes bibliographical references and indexes |
| Notes |
Master and use copy. Digital master created according to Benchmark for Faithful Digital Reproductions of Monographs and Serials, Version 1. Digital Library Federation, December 2002. http://purl.oclc.org/DLF/benchrepro0212 MiAaHDL |
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Print version record |
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digitized 2010 HathiTrust Digital Library committed to preserve pda MiAaHDL |
| Subject |
Diabetes -- Molecular aspects
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Diabetes Mellitus, Type 1 -- genetics
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Autoimmune Diseases -- immunology
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Diabetes Mellitus, Type 1 -- immunology
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Diabetes -- Molecular aspects
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Diabetes mellitus type 1.
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Moleculaire biologie.
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Pathologie.
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Diabetes mellitus
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Typ 1
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Molekularpathologie
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Aufsatzsammlung
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Molekulare Medizin
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| Form |
Electronic book
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| Author |
Von Herrath, Matthias G
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S. Karger (Firm)
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| ISBN |
9783318007152 |
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3318007153 |
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