Interactions between the immune system and connective tissue in arthritis: aspects on T-cell activation.
The synovial inflammation in rheumatoid arthritis can both serve as a model for the study of chronic inflammation in general and be analyzed with the goal to understand which features that distinguish RA from other chronic inflammatory diseases. In this paper we discuss both these problems with the emphasis on mechanisms of T cell activation and how activation of T cells against structures associated with the cartilage may contribute to the perpetuation of RA by means of triggering rheumatoid factor production. We also present some original data concerning phenotypes of in vivo activated synovial T cells, demonstrating high levels of HLA-DR expression, low levels of CD45+/Leu3a+ T "suppressor/inducer" cells and varying numbers of Leu 15+/Leu2a+ "suppressor" T cells. The observed phenotypic pattern is compatible with the occurrence of a normal but perpetuated immune response to a persistant antigen "X" in the arthritic joint.