Patients with rheumatoid arthritis have been studied in an attempt to detect immune responses to cartilage antigens that might function in the causation and/or perpetuation of joint inflammation. Cartilagenous antigenic determinants could be consistently demonstrated in synovial fluid and its phagocytic cellular components. Antibody to such constituents could not be detected in serum, synovial fluid or immunoglobulin eluted from or synthesized de novo by rheumatoid synovium. However, delayed hypersensitivity to cartilage antigens correlating with clinical evidence of inflammatory cartilagenous degradation could be identified.
Spontaneously released and T cell mitogen augmented lymphokine produced by human mononuclear cells has been shown to induce a concentration dependent reversible suppression of chondrocyte glycosaminoglycan and protein synthesis without significantly enhancing chondrocyte catabolic activity. The modulatory factor(s) is of T cell origin and is trypsin, pronase, and heat sensitive. Prostaglandin inhibitors failed to influence factor formation or activity. Although eluting from Sephadex G-100 over a wide range, peak activity had an approximate molecular weight of 53,000 and appeared distinct from recognized forms of lymphotoxin.Mounting evidence, albeit largely circumstantial, has implicated cell mediated immunologic mechanisms in the pathogenesis of human and experimental animal models of articular disease. Thus the predominant mononuclear cell infiltrating synovial membranes and that present in synovial fluids secured from distinct
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