British Journal of Rheumatology 1985;24(suppl 1):175—178 STIMULATION OF PRODUCTION OF INTERLEUKIN-1 AND AN INTERLEUKIN-1 INHIBITOR IN HUMAN MONOCYTES

Intcrlcukin (IL-1) production in human monocyles was examined in response to stimulation by different moleculai forms of bacterial lipopolysacchandes (LPS), recombinant human gamma interferon (IFN-y) and vanous forms ol immune complexes with or without complement. Stimulation of IL-1 production by LPS was enhanced by the presence of the 2-keto-3-deoxyoctonate (KDO) moiety as well as by diphosphoryl lipid A. IFN-Y alone did not induce IL-1 production but enhanced the stimulatory effects of LPS. Various forms of immune complexes, in the absence of detectable LPS contamination and of complement, failed to stimulate IL-1 production. Complement fixation by immune complex precipitates led to induction of IL-1 synthesis and secretion. Monocytes cultured on adherent immune complexes produced a specific IL-1 inhibitor KEY WORDS. Intcrleukin-1, Human monocytes, immune complexes PRODUCTION of interleukin-1 (IL-1) by human monocytes may be stimulated by various substances that these cells encounter in disease states. Bacterial lipopolysaccharides (LPS) will induce IL-1 production in concentrations as low as 10 pg/ml but the responsible molecular structures have not been determined (1,2). Gamma interferon (IFN-y) activates macrophages to exhibit many enhanced functions but the effects of IFN-y on IL-1 production are not known. Monocytes and macrophages encounter different forms of immune complexes in human diseases, possibly inducing IL-1 production (3)