Human alveolar macrophage suppression of lymphocyte proliferation. Accessory characteristics for the generation and functional expression of con A-induced suppressor cells.

Human alveolar macrophages (AM) provide less accessory support for mitogen- and antigen-stimulated lymphocyte proliferation than do autologous blood-derived macrophages (BM). This is at least in part due to suppression mediated by AM, but the mechanism of such suppression is not understood. To determine whether AM-mediated suppression is related to AM interaction with suppressor lymphocytes (Ts), we examined the accessory cell function of both AM and BM for the generation and functional expression of Ts induced by concanavalin A (Con A). The data indicate that human AM are equivalent to BM for the generation of Con A-induced Ts, but AM mediate less suppression of Con A-induced Ts, once generated, than do BM. Addition of indomethacin did not increase lymphocyte proliferation when AM served as accessory cells. Supernatant fluids of Con A-exposed AM promoted greater proliferation of human T-lymphocytes and mouse thymocytes than did supernatant fluids from Con A-exposed BM. Interleukin-1 inhibitor activity was not detected in the supernatant fluids. These observations make it unlikely that soluble factors alone account for AM-mediated suppression. Thus, at least for the Con A-induced Ts system, AM do not mediate suppression either via better generation or greater functional expression of suppressor cells relative to BM. The paradoxically greater proliferation of lymphocytes stimulated by the supernatant fluids of Con A-exposed AM raises the possibility that suppression of Con A-stimulated lymphocyte proliferation observed when AM serve as the accessory cells in primary culture may be related to AM secretion of a molecule with IL-1-like activity.