Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory condition that affects approximately 0.8% of the world population [1,2]. Although there are frequent systemic manifestations of inflammation, the primary physiological events occur within the synovial tissue lining of diarthrodial joints. In spite of intense investigation, the cause of RA and the precise pathophysiological events remain uncertain. Much attention has focused on T lymphocytes and the role they play in the pathogenesis of RA. Along with functional analyses of T cell populations, the mechanisms by which T cells enter rheumatoid synovium has been the focus of considerable investigation. A number of studies have demonstrated an essential role for cell surface adhesion receptors in T cell migration, although the specific receptors employed by T cells and their counterreceptors on endothelial cells have not been completely delineated. Postcapillary venules appear to be the site of T cell entry into the synovium, although this conclusion is based more on analogy to other tissue sites rather than direct experimental verification in the synovium.
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Oppenheimer-Marks, N., Lipsky, P.E. (1998). Adhesion molecules in arthritis: Control of T cell migration into the synovium. 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_7
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