Anergy in sarcoidosis: the role of interleukin-1 and prostaglandins in the depressed in vitro lymphocyte response.
We have shown that peripheral blood monocytes from patients with sarcoidosis release reduced amounts of interleukin-1 (IL-1) when compared with normals. In part, this defect explains the relative in vitro unresponsiveness of T lymphocytes from patients with sarcoidosis as measured by mitogen- or antigen-induced lymphocyte transformation. The addition of supernatants containing pre-formed IL-1 partially restored this defect. This enhancement was found to be additive to the previously described effect of indomethacin, an inhibitor of prostaglandin synthesis. Thus, it would appear that the activated peripheral blood monocytes found in sarcoidosis not only cause reduced lymphocyte proliferation by acting as suppressor cells but are also unable to act as accessory cells in producing IL-1.
D000328:Adult; D000368:Aged; D003208:Concanavalin A / Q000494:pharmacology; D015232:Dinoprostone; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007375:Interleukin-1 / Q000096:biosynthesis / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008171:Lung Diseases / Q000276:immunology*; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D011458:Prostaglandins E / Q000494:pharmacology*; D012507:Sarcoidosis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D007375:Interleukin-1; D008070:Lipopolysaccharides; D011458:Prostaglandins E; D003208:Concanavalin A; D015232:Dinoprostone; D007213:Indomethacin