We have previously shown that peripheral blood monocytes from HIV-infected patients constitutively produce IL-1 alpha and beta AIDS, 1989, 3, 695). In the present study, we observed that monocytes from HIV+ donors cultured in the presence of autologous T lymphocytes release less IL-1 activity (as assessed by a comitogenic assay) than purified monocytes cultured in the absence of T cells, without affecting the amount of released IL-1 protein. Inhibition of release of IL-1 activity was also observed when autologous T lymphocytes were added to cultures of LPS-stimulated monocytes from healthy seronegative individuals. The inhibitory effect of T cells required homotypic interactions between T cells and monocytes and was also observed by adding supernatants from PHA-stimulated T cells to monocytes in culture. Inhibition was not observed with purified CD8+ lymphocytes. Inhibition mediated by T cells was dependent on the induction of the production and release by monocytes of the functional inhibitor of IL-1, IL-1 Ra, as assessed by ELISA. Induction by T cells of IL-1 Ra release was not dependent on the production of TGF beta. These observations indicate that CD4+ T lymphocytes negatively regulate the activity of released IL-1 by stimulated monocytes and suggest that the loss of CD4 cells in HIV disease enhances the proinflammatory effects of IL-1 that is constitutively produced by monocytes of infected patients.

*CD4-Positive T-Lymphocytes/IMMUNOLOGY *HIV Infections/IMMUNOLOGY *Interleukin-1/METABOLISM *Sialoglycoproteins/SECRETION

www.aegis.org