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Interleukin‐1 Production by Blood Monocytes and Bronchoalveolar Cells in Sarcoidosis

Hypersensitivity to antigen is a cell-mediated immune response that is readily assessed in vivo by skin testing and in vitro by observing lymphocyte blastogenesis. In sarcoidosis depressed antigen reactivity is frequently observed both in in vivo' and in vitro2 studies and contrasts with local activation of cellular immune responses in the lung, skin, and other organs as evidenced by lymphocytic infiltration and granuloma f~rmation.~ The immune mechanisms underlying systemic anergy in sarcoidosis are poorly understood. Immunosuppressive serum factors have been demonstrated in some sarcoidosis patients: and excessive production of immunosuppressive cyclooxygenase products of arachidonic acid by blood monocytes has been reported? Although these observations suggest that anergy in sarcoidosis is caused by suppressor factors, alterations in antigen-responding thymus-derived (T) cells or mononuclear phagocyte immune accessory function may have contributory effects. A deficiency of circulating T lymphocytes has been reported by some investigators: and recent studies demonstrating a reciprocal distribution of the T helper-inducer subpopulation in the lung and peripheral blood suggests that T helper-inducer cells may be selectively recruited from the circulation.' Mononuclear phagocytes have a pivotal role in the induction of the immune response to antigen, and production of the growth factor interleukin-1 (IL1) is critical to the ability of monocytes/macrophages to function as immune accessory cells.' The objective of this study of sarcoidosis was to examine IL-1 production by blood monocytes and alveolar macrophages in order to determine if a deficiency in the production of this growth factor could contribute to the depression of antigen responses.