J.J. Goronzy / C.M. Weyand (eds.)

Rheumatoid Arthritis

Mitwirkender: Weyand, C. M.; Goronzy, J. J.

• Gebundenes Buch

Produktbeschreibung

Rheumatoid arthritis is a crippling disease, affecting individuals in the prime of their life. This disease is emerging as a paradigm for complex autoimmune syndromes in which multiple genetic risk determinants in combination with non-inherited factors predispose individuals to generate chronically persistent and destructive immune responses. As a consequence of exploring the immunopathology of rheumatoid arthritis, biologic response modifiers have been introduced as a fundamental new therapeutic strategy for this clinically challenging disease. This book, the third volume of the new series 'Current Directions in Autoimmunity', is the first one to exclusively focus on one disease. Written by experts in genetics and immunobiology, the articles reflect the complexity and multiple facets of the disease process but also show their convergence to a better understanding of pathogenetic mechanisms and the evolving clinical applications. The models and concepts described in this volume have implications for studies of other inflammatory diseases and are of interest not only for clinical and basic scientists devoted to the study of rheumatoid arthritis but for investigators of autoimmune diseases in general.

Produktdetails

• Current Directions in Autoimmunity
• Verlag: Karger
• Seitenzahl: 282
• Englisch
• Abmessung: 250mm
• Gewicht: 744g
• ISBN-13: 9783805571203
• ISBN-10: 3805571208
• Artikelnr.: 27561562

Autorenporträt

Goronzy, J.J.; Weyand, C.M. (Rochester, Minn.)

Inhaltsangabe

1;Contents;6
2;Prologue;8
3;Susceptibility Genes in Rheumatoid Arthritis;10
3.1;The Genetic Predisposition to RA Is Only Partially Explained by HLA;11
3.2;RA Is Being Investigated by Both Approaches;15
3.3;Conclusion and Perspectives;19
3.4;Acknowledgments;20
3.5;References;20
4;Elucidation of Pathways Leading to Rheumatoid Arthritis by Genetic Analysis of Animal Models;26
4.1;Genetic Influence on Rheumatoid Arthritis;26
4.2;Animal Models;28
4.3;Identiflcation of Genes and Their Pathogenic Role;39
4.4;Acknowledgments;40
4.5;References;40
5;Structural Basis for the HLA-DR Association of Rheumatoid Arthritis;45
5.1;Peptide-HLA-DR Molecule Interaction;46
5.2;Class II Binding Motifs;47
5.3;QuantitativeMatrices and the Computational Prediction of HLA-DR-Peptide Binding;48
5.4;Peptide-Binding Specificities and RA-Associated HLA Class II Molecules;49
5.5;How to Translate the HLA-DR Association of RA into Disease Mechanisms?;50
5.6;Prospects for Immunointervention;55
5.7;Concluding Remarks;56
5.8;References;57
6;T Cell Repertoire Formation and Molecular Mimicry in Rheumatoid Arthritis;60
6.1;Recognition of Self Is the Driving Force in Thymic Selection;61
6.2;Thymic Selection Is a Dynamic and Adaptable Process;62
6.3;A Self-MHC-Derived Peptide Contributes to Positive Selection of T Cells Which Are Cross-Reactive with a Homologous Foreign Antigen;63
6.4;Rheumatoid Arthritis;64
6.5;Environmental Factors: Heat Shock Proteins Are a Group of the Antigenic Proteins in Autoimmune Arthritis;64
6.6;Genetic Factors: Shared Epitope in RA;65
6.7;The Multistep Mimicry Hypothesis;66
6.8;Microbial Peptides Activate Shared Epitope-Specific T and Induce Production of Proinflammatory Cytokine Cells in RA Patients: A Dangerous Aberration from Physiological Homeostasis?;66
6.9;Self Shared Epitope Peptides Shape and Maintain a Repertoire of T Cells Cross-Reactive with Foreign Homologues;68
6.10;Conclusion;69
6.11;Acknowledgments;70
6.12;References;70
7;Exploring the Pathogenesis of Rheumatoid Arthritis in Transgenic and Mutant Mice;73
7.1;Exploring HLA-DR4-Restricted T Cell Responses in vivo;74
7.2;Is Systemic Autoreactivity Sufficient to Induce Joint-Speci.c Autoimmunity?;84
7.3;The Effector Phase of Inflammatory Arthritis;87
7.4;Predicting the Progression through Disease Checkpoints in the Non-Susceptible Host;93
7.5;Future Directions;97
7.6;Acknowledgments;98
7.7;References;98
8;Molecular Mimicry and Lyme Arthritis;103
8.1;Causative Agent;104
8.2;Disease Vector;104
8.3;Clinical Picture;105
8.4;Antibiotic Treatment-Resistant Lyme Arthritis;105
8.5;HLA Association with Autoimmune Diseases;106
8.6;Treatment-Resistant Lyme Arthritis and Immunity to OspA;107
8.7;LFA-1 as a Candidate Autoantigen in Treatment-Resistant Lyme Arthritis;109
8.8;Variations in OspA Sequences in European and Asian Strains;111
8.9;The Pathogenic Model;112
8.10;Animal Models of Lyme Arthritis;114
8.11;Implications beyond Lyme Disease;115
8.12;References;116
9;T Cell Homeostasis and Autoreactivity in Rheumatoid Arthritis;121
9.1;Introduction;121
9.2;RA A Disease of Systemic Autoimmunity with Predominant Joint Involvement;122
9.3;Defective Central Tolerance in Murine Models of RA;122
9.4;The T Cell Repertoire in RA;124
9.5;Clonal Expansion of Autoreactive T Cells in RA;125
9.6;T Cell Repertoire Contraction in RA;126
9.7;T Cell Population Dynamics Murine Studies;129
9.8;T Cell Population Dynamics in Humans;131
9.9;T Cell Population Dynamics in RA;132
9.10;Emergence of CD28 T Cells in RA;134
9.11;Therapeutic Implications of Abnormal T Cell Homeostasis in RA;135
9.12;Conclusions;136
9.13;Acknowledgment;138
9.14;References;138
10;Leukocyte Homing to Synovium;142
10.1;Pathways of Leukocyte Migration;142
10.2;Regulation of Homing to Inflamed Synovium;157
10.3;Conclusion;164
10.4;Acknowledgments;165
10.5;References;165
11;Lymphoid Microstructures in Rheumatoid Synovitis;177
11.1;Introduction;177
11.2;CD4 T Cells Ar