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T Cells as primary players in rheumatoid arthritis

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T Cells in Arthritis

Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

The sequence of events required for the development of rheumatoid arthritis (RA) remains poorly defined. Evidence strongly supports a genetic predisposition for disease development, and an association between certain class II major histocompatibility complex (MHC) alleles and the development and severity of RA has been established. Clearly, environmental factors are also likely to contribute to the disease process, although these etiological agents in RA have not been identified. Early histopathological alterations in the RA joint include morphological and phenotypic changes in the vascular endothelium, and hypertrophy of the synovial lining cells. However, also present at this stage is a modest perivascular accumulation of lymphocytes, including T lymphocytes. As disease progresses, this T cell infiltration becomes more pronounced and frequently more organized, and is accompanied by an influx of B lymphocytes, macrophages, dendritic cells and fibroblasts. Cytokines, primarily of macrophage and fibroblast origin, are secreted in abundance within the synovia and contribute in multiple ways to the progression of chronic inflammation, synovial cell proliferation and expansion, and cartilage destruction.

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Falta, M.T., Kotzin, B.L. (1998). T Cells as primary players in rheumatoid arthritis. In: Miossec, P., Firestein, G.S., van den Berg, W.B. (eds) T Cells in Arthritis. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8823-3_11

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