Cellular sensitivity to collagen in rheumatoid arthritis.
Using an assay to measure antigen-induction of a lymphocyte mediator, LIF, we detected cellular sensitivities to native human types II and III collagens in three-quarters of a group of 50 patients with rheumatoid arthritis. There was no cellular response to type I collagen. Cellular reactivities to collagen were absent in a group of 41 patients who had other kinds of arthritis, such as osteoarthritis, crystalline-induced synovitis, or arthropathies associated with a high prevalence of the HLA-B27 antigen. Lymphocytes, responding to an unknown persistent antigenic stimulus, are thought to play a major role in the pathogenesis of rheumatoid arthritis. It has previously been hypothesized that collagen might function as an autoantigen in this disease. Based on the disease specificity of our findings and the tissue distribution of types II and III collagens, we propose that cellular sensitivities to these structural proteins may be involved in the pathogenesis of rheumatoid arthritis.
D000328:Adult; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D001327:Autoimmune Diseases / Q000276:immunology; D003094:Collagen / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D008222:Lymphokines / Q000276:immunology; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology; D010003:Osteoarthritis / Q000276:immunology; D011691:Puromycin / Q000494:pharmacology
D008222:Lymphokines; D011691:Puromycin; D003094:Collagen