Strategies for medical treatment based on current understanding of the pathogenesis of rheumatoid arthritis.
Although empiric principles still govern most therapies available for patients with rheumatoid arthritis (RA), strategies for the medical management of RA are beginning to be appreciated in terms of their actions on pathogenetic mechanisms relevant for this disease. Evidence suggests that anti-self-reactivity is central to the perpetuation of the articular manifestations of RA and that this autoimmune process is subserved, at least in part, by T cells. Data exist indicating that therapies effective in ameliorating RA inhibit T-cell replication and function. Experimental studies have provided results that, at present, are inconclusive in terms of the degree of clinical efficacy, but these trials have shown further that methods capable of influencing T cells are promising for the future treatment of this disease.
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007975:Leukotriene B4 / Q000276:immunology; D008212:Lymphocyte Depletion; D015846:Monokines; D010956:Plasmapheresis; D011506:Proteins / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D000893:Anti-Inflammatory Agents; D001323:Autoantibodies; D005938:Glucocorticoids; D007074:Immunoglobulin G; D015846:Monokines; D011506:Proteins; D007975:Leukotriene B4