Chapter category: Autoimmunity
CTLA-4 in Rheumatoid Arthritis
CTLA-4 in Autoimmune Disease
Edited by: Flemming PociotISBN: 1-58706-068-X
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Chapter authors:
Peter P. Sfikakis and Stamatis-Nick Liossis
Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease characterised by symmetric polyarthritis of the small joints of the hands and feet and the larger appendicular joints. The etiology of RA is still unknown. Although several features of autoimmunity are prominent in these patients, the nature of the antigen(s) driving joint inflammation remains unclear. While the initiation phase of RA might result from an (auto)antigen-specific T cell response, the perpetuation of inflammation leading to joint destruction in the late chronic phases of the disease is a consequence of complex pathogenetic mechanisms involving aberrant interactions between T cells, macrophages, and synovial fibroblasts. T cells are the most frequently observed inflammatory cell in the rheumatoid joint (1-3). Not all authorities agree that RA is a purely T cell-mediated disease; however, an important pathogenetic role of the T cells has been clearly established. Besides their frequency, the fact that the majority possess both a memory and an activated T cell phenotype, as well as the association of RA with specific molecules of the major histocompatibility complex (MHC) class II underscore the central role of T cells in the pathogenesis of RA.3,4 Two signals are necessary for a productive T cell stimulation which is required for all T cell-dependent immune processes. The first signal confers specificity and is transduced via the T cell-surface antigen receptor (TCR) when antigen is properly presented to the T cell by an antigen
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