Activated Inflammatory T Lymphocytes in Rheumatoid Synovitis — Effect of Cyclosporine A and Anti-Tac
One of the characteristic features in rheumatoid arthritis (RA) is a chronic inflammation with an extensive infiltration of lymphocytes in the synovitis in the joints of these patients. Immunohistological studies of rheumatoid synovitis have revealed that the infiltrating cells are organized in follicles-like structures with inflammatory T cells of the CD4 phenotype localized in close contact with strongly HLA-DR positive, dendritic-like cells (2,3). A similar infiltration of plasma cells have also been described (4). In recent studies some investigators have reported that synovial tissue (ST) and synovial fluid (SF) T lymphocytes are activated as shown by high incorporation of 3H-labelled thymidine, and by expression of various activation markers (5,6). In contrast, other investigators have reported a defective T cell system in RA patients as shown by low or deficient production of interleukin 2 (IL-2) (7). Very recent studies have shown that lymphoid dendritic cells (DC) isolated from inflammatory sites like the ST and SF are very potent stimulators of T cells in autologous and allogeneic mixed leucocyte reaction (MLR) and are very effective accessory cells for antigenic and mitogenic T cell responses (8,9,10). To assess whether the rheumatoid patients have a defective or an activated T cell system, inflammatory T cells from rheumatoid synovitis were compared with normal T cells activated by blood DC in autologous MLR with respect to activation markers, and to production and consumption of IL-2.
KeywordsDendritic Cell Rheumatoid Arthritis Patient Synovial Fluid Synovial Tissue Normal Peripheral Blood
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