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Rheumatoid arthritis (RA) is the most common and most severe form of inflammatory arthritis. The pathogenesis of RA has been the subject of intense research for several decades. The prevailing hypotheses have changed over the years, and have attempted to incorporate the most recent data. Although T cells represent an important component of the cells which infiltrate the joint synovium, their contribution at a late stage of the disease remains a matter of debate. The goal of this book is to outline the major arguments and data suggesting that T cells may, or may not, be central players in the pathogenesis of chronic RA. While each of the editors and authors has his/her own bias (as will be clear by reading the respective chapters), our hope is that the readers will enjoy a complete and balanced view of the critical questions and experiments. This is not just an intellectual exercise since the direction of future therapeutic interventions depends heavily on how one interprets the pathogenesis of RA and the contribution of T cells.
List of contents
T Cells as Secondary Players in Rheumatoid Arthritis.- T cell receptor rearrangements in arthritis.- T cell-independent joint destruction.- Role of T cells in arthritis: Lessons from animal models.- The Th1/Th2 cytokine balance in arthritis.- Interactions between T cell plasma membranes and monocytes.- Adhesion molecules in arthritis: Control of T cell migration into the synovium.- T cell reactivity to Epstein-Barr virus in rheumatoid arthritis.- T cell responses in reactive and Lyme arthritis.- T cell directed therapies and biologics.- T cells as primary players in rheumatoid arthritis.
Summary
Rheumatoid arthritis (RA) is the most common and most severe form of inflammatory arthritis. The pathogenesis of RA has been the subject of intense research for several decades. The prevailing hypotheses have changed over the years, and have attempted to incorporate the most recent data. Although T cells represent an important component of the cells which infiltrate the joint synovium, their contribution at a late stage of the disease remains a matter of debate. The goal of this book is to outline the major arguments and data suggesting that T cells may, or may not, be central players in the pathogenesis of chronic RA. While each of the editors and authors has his/her own bias (as will be clear by reading the respective chapters), our hope is that the readers will enjoy a complete and balanced view of the critical questions and experiments. This is not just an intellectual exercise since the direction of future therapeutic interventions depends heavily on how one interprets the pathogenesis of RA and the contribution of T cells.
