附註:Includes bibliographical references and indexes.
Prologue -- Susceptibility genes in rheumatoid arthritis -- Elucidation of pathways leading to rheumatoid arthritis by genetic analysis of animal models -- Structured basis for the HLA-DR association of rheumatoid arthritis -- T cell repertoire formation and molecular mimicry in rheumatoid arthritis -- Exploring the pathogenesis of rheumatoid arthritis in transgenic and mutant mice -- Molecular mimicry and lyme arthritis -- T cell homeostasis and autoreactivity in rheumatoid arthritis -- Leukocyte homing to synovium -- Lymphoid microstructures in rheumatoid synovitis -- The role of TNF[alpha] and IL-1 in rheumatoid arthritis -- Innate response cytokines in inflammatory synovitis: a role for interleukin-15 -- Regulation of apoptosis of synovial fibroblasts -- Biologics in the treatment of rheumatoid arthritis: mechanisms of action.
摘要: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.
