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Current Concepts in Autoimmunity and Chronic Inflammation

E-BookPDF1 - PDF WatermarkE-Book
282 Seiten
Englisch
Springer Berlin Heidelbergerschienen am08.09.20062006
The immune system has been known to be capable of distinguishing self from non-self since the pioneering work of Paul Erhlich more than a century ago. Originally described in experiments studying blood transfusion comp- ibility, the principle of 'horror autotoxicus' is still valid, although today the phenomenon is usually described in terms of tolerance or ignorance. A great deal has been learned about the various processes preventing self-reactivity normally. These include processes that operate during immune cell ontogeny and subsequently on reactivity of mature lymphocytes in the periphery. They encompass mechanisms that are intrinsic to potentially reactive lymphocytes and can result in central or peripheral deletion or the alteration of functional potential. In addition, there are in?uences that are extrinsic to potentially auto-reactive lymphocytes, including the function of regulatory cells, d- ferentiation state of antigen-presenting cells, availability of self-antigen, the cytokine and chemokine milieu, as well as the traf?cking patterns involved in generating productive immune interactions. It is clear that the immune system devotes a considerable effort to the avoidance of the development of potentially pathogenic self-reactivity. Despite this, the development of self-reactivity is relatively common. - though the development of autoimmune disease is less frequent, autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, systemic lupus e- thematosus, psoriasis, thyroiditis, and myasthenia gravis, are all too common, and can cause considerable morbidity and even mortality.mehr
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Produkt

KlappentextThe immune system has been known to be capable of distinguishing self from non-self since the pioneering work of Paul Erhlich more than a century ago. Originally described in experiments studying blood transfusion comp- ibility, the principle of 'horror autotoxicus' is still valid, although today the phenomenon is usually described in terms of tolerance or ignorance. A great deal has been learned about the various processes preventing self-reactivity normally. These include processes that operate during immune cell ontogeny and subsequently on reactivity of mature lymphocytes in the periphery. They encompass mechanisms that are intrinsic to potentially reactive lymphocytes and can result in central or peripheral deletion or the alteration of functional potential. In addition, there are in?uences that are extrinsic to potentially auto-reactive lymphocytes, including the function of regulatory cells, d- ferentiation state of antigen-presenting cells, availability of self-antigen, the cytokine and chemokine milieu, as well as the traf?cking patterns involved in generating productive immune interactions. It is clear that the immune system devotes a considerable effort to the avoidance of the development of potentially pathogenic self-reactivity. Despite this, the development of self-reactivity is relatively common. - though the development of autoimmune disease is less frequent, autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, systemic lupus e- thematosus, psoriasis, thyroiditis, and myasthenia gravis, are all too common, and can cause considerable morbidity and even mortality.
Details
Weitere ISBN/GTIN9783540297147
ProduktartE-Book
EinbandartE-Book
FormatPDF
Format Hinweis1 - PDF Watermark
FormatE107
Erscheinungsjahr2006
Erscheinungsdatum08.09.2006
Auflage2006
ReiheCurrent Topics in Microbiology and Immunology
Reihen-Nr.305
Seiten282 Seiten
SpracheEnglisch
IllustrationenIX, 282 p.
Artikel-Nr.1424720
Rubriken
Genre9200

Inhalt/Kritik

Inhaltsverzeichnis
1;Preface;5
2;List of Contents;7
3;List of Contributors;9
4;B Cell Tolerance-How to Make It and How to Break It;10
4.1;1 Introduction;11
4.2;2 Repertoire Selections by the pre-B Cell Receptor;15
4.3;3 Generation of Immature, sIgM+ B Cells;16
4.4;4 Negative and Positive Selection, and Ignorance of the Developing Immature B Cell Repertoires;18
4.5;5 Negative Selection and Editing;19
4.6;6 Ignorance;21
4.7;7 Positive Selection;22
4.8;8 Peripheral B CellsWithout sIg Expression;23
4.9;9 Rescue of Autoreactive B Cells by T Cell-Independent Antigens of Type I, TLR- Ligand- Antigen- Complexes;24
4.10;10 Autoreaction Rescued by Ignorance;25
4.11;11 Breaking the Tolerance ofMature, Peripheral B Cell Repertoires;26
4.12;12 Consequences of Breaking B Cell Tolerance-Autoimmune Diseases;28
4.13;References;29
5;Breaking Ignorance: The Case of the Brain;34
5.1;1 Introduction;35
5.2;2 Brain Autoantigens in the Immune System;36
5.3;3 B Cell Ignorance?;39
5.4;4 Activation of Ignorant Autoreactive T Cells- The Transition from Autoreactive to Autoaggressive;41
5.5;5 Regulatory Suppression of Autoimmune T Cells- But How Do Suppressor T Cells Know?;47
5.6;6 Conclusion;53
5.7;References;54
6;Naturally Arising Foxp3-Expressing CD25+ CD4+ Regulatory T Cells in Self- Tolerance and Autoimmune Disease;60
6.1;1 Introduction;61
6.2;2 Self-Tolerance Maintained by Thymus-Produced Natural Treg: Induction of Autoimmune Disease by Their Manipulation at the Cellular and Molecular Level;62
6.3;3 IPEX as an Example of Human Autoimmune Disease Due to a Genetic Defect of Naturally Arising CD25+ CD4+ Treg: Its Implications for Immunologic Self- Tolerance and Autoimmune Disease in Humans;66
6.4;4 Contribution of Impaired Immunoregulation and Host Genetic Factors to the Development of Autoimmune Disease: A Possible Mechanism of Autoimmune Disease;67
6.5;5 Conclusion and Perspective;71
6.6;References;71
7;Sex Hormones and SLE: Influencing the Fate of Autoreactive B Cells;76
7.1;1 Introduction;77
7.2;2 Estrogen, Prolactin, and B Cell Fate in the R4A Model;83
7.3;3 Clinical Relevance;88
7.4;4 Conclusion;89
7.5;References;90
8;Innate (Over)immunity and Adaptive Autoimmune Disease;98
8.1;1 Introduction;98
8.2;2 Autoimmunity and/or Infection;99
8.3;3 Innate Regulators of Autoreactive T Cell Priming;102
8.4;4 Regulatory T Cells and Their Relation to Toll-Like Receptor Signals;104
8.5;5 Lack of (Auto)immunity After Innate Overactivation: A Role for Interferons and the Nervous System;105
8.6;6 Autoreactivity and Conversion to Autoimmune Disease;106
8.7;7 Conclusion;108
8.8;References;109
9;Can Unresolved Infection Precipitate Autoimmune Disease?;114
9.1;1 Introduction;115
9.2;2 Crohn s Disease;116
9.3;3 Ankylosing Spondylitis and the Other Spondyloarthritides;121
9.4;4 Regulatory Mechanisms in Autoimmunity;124
9.5;References;127
10;The Systemic Autoinflammatory Diseases: Inborn Errors of the Innate Immune System;136
10.1;1 Introduction;137
10.2;2 Familial Mediterranean Fever;139
10.3;3 Syndrome of Pyogenic Arthritis, Pyoderma Gangrenosum, and Acne;142
10.4;4 The Cryopyrinopathies: Familial Cold Autoinflammatory Syndrome, Muckle- Wells Syndrome, and Neonatal- Onset Multisystem Inflammatory Disease;144
10.5;5 Blau Syndrome;148
10.6;6 TNF Receptor-Associated Periodic Syndrome;150
10.7;7 Hyperimmunoglobulinemia D with Periodic Fever Syndrome;154
10.8;8 Concluding Remarks;157
10.9;References;158
11;Inefficient Clearance of Dying Cells and Autoreactivity;170
11.1;1 The Comeback of Dying Cells;171
11.2;2 Various Molecules Are Involved in the Clearance of Dying Cells;172
11.3;3 C-Reactive Protein and Dying Cells;173
11.4;4 Complement and DNase I Act as Back-up Molecules in the Clearance Process;174
11.5;5 Phosphatidylserine Exposure as One Early Membrane Change of Apoptotic Cells;174
11.6;6 Changes in the Glycoprotein Composition of Membranes of Apoptotic Cells;175
11.7;7 Impaired Clearance Functions and Autoimmunity;177
11.8;8 Heterogeneous and Intrinsic Clearance Defects in Some SLE Patients;179
11.9;9 Conclusion;180
11.10;References;180
12;The Importance of T Cell Interactions with Macrophages in Rheumatoid Cytokine Production;186
12.1;1 Introduction;187
12.2;2 Cognate-Dependent Interactions;189
12.3;3 Macrophage Lineage;193
12.4;4 Concluding Remarks;195
12.5;References;195
13;T Cell Activation as Starter and Motor of Rheumatic Inflammation;204
13.1;1 T Cell Development and T Cell Subsets;205
13.2;2 CD4 T Cells in Rheumatic Inflammation;208
13.3;3 The Th1/Th2 Dichotomy;209
13.4;4 Rheumatic Inflammation Is Driven by Activated Th1 Cells;211
13.5;5 T Cell-Directed Therapies;213
13.6;6 Conclusion;216
13.7;References;217
14;Signalling Pathways in B Cells: Implications for Autoimmunity;222
14.1;1 Introduction;223
14.2;2 Disturbed Homeostasis of Peripheral B Cells in Autoimmune Diseases;225
14.3;3 B Cellular Signal Transduction Pathways and Their Implications for Autoimmunity;227
14.4;4 Inhibitory Receptor Pathways and Autoimmunity;237
14.5;5 Activated B Cells May Bridge the Innate and Adaptive Immune System;239
14.6;6 Rationales of B Cell-Targeted Therapy in Autoimmune Diseases;240
14.7;References;243
15;Immunological Memory Stabilizing Autoreactivity;250
15.1;1 Mechanisms Contributing to Autoimmune Diseases;251
15.2;2 Immunological Memory and Chronic Autoimmune Diseases;252
15.3;3 Autoreactive Memory and Chronic Inflammation;258
15.4;References;260
16;Genetics of Autoimmune Diseases: AMultistep Process;268
16.1;1 Introduction;269
16.2;2 Definition of Autoimmune Disease: Physiology Versus Pathology;269
16.3;3 From Genes to Disease: The Basic Science Approach;271
16.4;4 FromDisease to Genes: The Monogenic Success and the Polygenic Failure;271
16.5;5 The Use of Animal Models in a Disease-to-Gene Approach;273
16.6;6 Positional Cloning of Ncf1, a Genetic Polymorphism Explaining aMajor Quantitative Trait Locus Controlling Chronic Inflammation;274
16.7;7 The Ncf1 Protein and the NADPH Complex;276
16.8;8 Pathway Analysis;277
16.9;9 Therapeutic Possibilities Can Be Immediately Explored;279
16.10;10 Analyses of a QTL Containing Interacting Genes;279
16.11;11 Conclusions;282
16.12;References;282
17;Subject Index;286mehr