[Recent advance in polymyositis and dermatomyositis research].
Past paradigm that the muscle tissue injury is driven by CD4 T cells and associated humoral immunity in dermatomyositis (DM), and by cytotoxic T cells in polymyositis (PM) is now under challenge. Although pathogenic autoantigens are to be identified, skeletal muscle C-protein was an excellent immunogen to provoke experimental myositis mimicking human PM. Serum antibodies against aminoacyl tRNA synthases appear in PM/DM patients, but more often in interstitial pneumonitis patients. Inflammatory cytokines are obviously involved in the pathogenesis. Animal studies showed that autoimmune myositis occurs without tumor necrosis factor alpha. Indeed, its blockade has yielded inconsistent outcome. Most crucial ones will be therapeutic targets in the future.
Kohsaka
Hitoshi
H
Department of Medicine and Rheumatology, Graduate School, Tokyo Medical and Dental University.
D000604:Amino Acyl-tRNA Synthetases / Q000276:immunology; D000818:Animals; D001323:Autoantibodies; D001324:Autoantigens; D001402:B-Lymphocytes / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002352:Carrier Proteins / Q000276:immunology; D016207:Cytokines; D003882:Dermatomyositis / Q000276:immunology / Q000628:therapy; D006801:Humans; D017285:Polymyositis / Q000276:immunology / Q000628:therapy; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha; D000099163:Myosin Binding Protein C
D000604:Amino Acyl-tRNA Synthetases; D001323:Autoantibodies; D001324:Autoantigens; D002352:Carrier Proteins; D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D000099163:Myosin Binding Protein C