[T-lymphocytes--do they control rheumatic immune responses?].
T cells, in particular CD4(+) T cells, have been implicated in mediating many aspects of rheumatoid inflammation. In rheumatoid arthritis (RA), CD4(+) T cells display various functional abnormalities in the synovium as well as in the peripheral circulation. Current evidence suggests, however, that the role of CD4(+) T cells in the development of rheumatoid inflammation exceeds that of activated pro-inflammatory effector T cells that drive the chronic autoimmune response. Subsets of CD4(+) T cells with regulatory capacity, such as CD25(+) Tregs, have been identified in mice and man, and recent observations suggest that in RA, the function of these regulatory T cells is severely impaired. Thus, in RA, defective regulatory immune mechanisms might allow the breakdown of peripheral tolerance, following which the detrimental CD4(+) T-cell-driven immune response evolves and proceeds to chronic inflammation. Here, we review the functional abnormalities and the contribution of different T-cell subsets to rheumatoid inflammation.
Wagner
U
U
Medizinische Klinik und Poliklinik IV, Universität Leipzig, Liebigstrasse 22, 04103 Leipzig, Germany. wagu@medizin.uni-leipzig.de
Schulze-Koops
H
H
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000473:pathology*; D015551:Autoimmunity / Q000276:immunology*; D016207:Cytokines / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology*; D018448:Models, Immunological; D013601:T-Lymphocytes / Q000276:immunology*
D016207:Cytokines