T-cell-dependent pathways in rheumatoid arthritis.
Two theories, not necessarily mutually exclusive, attempt to explain the pathogenesis of rheumatoid arthritis. The mesenchymal hypothesis proposes that, after an initial event triggered by T cells, synovitis is maintained by autocrine and paracrine pathways involving macrophages and synovial fibroblasts. The T-cell hypothesis proposes that T cells are continuously involved in the pathogenesis of rheumatoid arthritis from its initiation phase through to the chronic stage. This paper reviews recent work in this area and concludes that there is substantial evidence in support of the T-cell hypothesis.
Panayi
G S
GS
Rheumatology Unit, United Medical School, Guy's Hospital, London, UK.
D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000503:physiopathology*; D001324:Autoantigens / Q000276:immunology; D016207:Cytokines / Q000235:genetics / Q000502:physiology; D006801:Humans; D007596:Joints / Q000503:physiopathology; D008954:Models, Biological; D013585:Synovitis / Q000209:etiology; D013601:T-Lymphocytes / Q000502:physiology*; D014158:Transcription, Genetic
D001324:Autoantigens; D016207:Cytokines