Recombinant human interleukin-1 beta (rhIL-1 beta) is shown to be a strong inducer of Fc receptors (FcR) on murine macrophages and not on granulocytes. Data is provided indicating that rhIL-1 beta does induce specific but not nonspecific phagocytosis. Macrophages are shown to autoinduce their FcR expression as a function of time in culture. This induction is increased by the use of exogenous rhIL-1 beta and inhibited by anti-rhIL-1 beta antibody, pointing to an autocrine regulation of FcR expression on macrophages. On the other hand the myelomonocytic cell line WEH13BD- and the macrophage like cell line WR19M.1 are also shown to be inducible for the expression of FcR by this molecule. Data is also provided showing that recombinant murine Interferon gamma (rmIFN gamma) induces FcR on both macrophages and granulocytes. Whereas polyclonal antibodies inhibit FcR induction by IL-1 on macrophages, it does not inhibit FcR induction by IFN gamma on these cells. This points to a different mechanism of induction of FcR by IFN and IL-1. Finally, the possible application of rhIL-1 beta in vivo to help the organism fight infections is discussed.