Rheumatoid arthritis: etiopathogenetic considerations.
Although the etiology of rheumatoid arthritis remains unknown, evidence accumulated in the past several years seems to suggest that pathogenetic mechanisms are multifactorial. Genetic predisposition, perhaps mediated by the HLA system, may render an individual susceptible to the action of an undefined microbial agent, most likely a virus, resulting in the triggering of an inflammatory reaction that, if unchecked, will lead to the development of synovitis and eventually to tissue destruction. It is quite possible that similar pathogenetic events play a role in some of the extra-articular manifestations of the disease, including Felty's and Sjögren's syndromes, and vasculitis. Further understanding of the mechanisms involved should improve our understanding of the disease process and may result in new therapeutic approaches.
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D001172:Arthritis, Rheumatoid / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D001424:Bacterial Infections / Q000150:complications; D003602:Cytotoxicity, Immunologic; D015804:HLA-DR4 Antigen; D000949:Histocompatibility Antigens Class II / Q000235:genetics; D006801:Humans; D007111:Immunity, Cellular; D007125:Immunogenetics; D012217:Rheumatoid Factor / Q000096:biosynthesis; D013601:T-Lymphocytes / Q000276:immunology; D014777:Virus Diseases / Q000150:complications
D015804:HLA-DR4 Antigen; D000949:Histocompatibility Antigens Class II; D012217:Rheumatoid Factor