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T cells as secondary players in rheumatoid arthritis

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T Cells in Arthritis

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

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Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects about 1% of the general population worldwide [1]. The pathogenesis of RA remains a subject of debate, and many paradigms have been proposed and disputed over the years. The concept of autoimmunity in RA appeared in the 1940’s when it was first appreciated that self-reacting antibodies (rheumatoid factors) are present in the blood of most patients with RA [2]. Subsequently, advances in immunological techniques established the framework for the “extravascular immune complex” hypothesis in the early 1970’s [3-5]. This theory speculated that the inflammatory response in RA is initiated by the local production of rheumatoid factors and/or antibody directed against an undefined antigen. This, in turn, leads to complement fixation and generation of chemotactic molecules that attract polymorphonuclear leukocytes into joints. Hydrolytic enzymes contained within lysozomal granules are then released during phagocytosis of immune complexes and mediate the destructive process in the RA joint [6]. However, many questions remain unanswered by this model, especially mechanisms of synoviocyte invasion into articular cartilage.

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Nguyen, K.H.Y., Firestein, G.S. (1998). T cells as secondary 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_1

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  • DOI: https://doi.org/10.1007/978-3-0348-8823-3_1

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