AbstractThe effect of interleukin 2 (IL 2) on the capability of human monocytes to secrete reactive oxygen species triggered via Fc‐γ receptor (Fc‐γ R) function had been investigated by measurement of chemiluminescence (CL). IL 2 did not activate highly purified (hp) monocytes to respond to Fc‐γ R mediated phagocytic stimulation with an enhanced respiratory burst activity unless low numbers of T cells had been co‐cultured with hp monocytes. Supernatants from IL 2 treated PBMC contained interferon‐γ (IFN‐γ) and monocyte activating factor (MAF) activity. The secretion of both cytokine activities was strongly enhanced by cooperative function of monocytes. The correlation of IL 2 induced secretion of IFN‐γ and MAF activity was striking, however, monoclonal antibody (mAb) anti‐human IFN‐γ failed to abrogate IL 2 stimulated and lymphocyte dependent monocyte activation. Although IL 2 had no direct monocyte activating effect, pretreatment of hp monocytes with IL 2 led to monocyte priming: subsequent co‐culture with autologous control T cells enhanced the monocyte Fc‐γ R mediated CL response. The priming of monocytes by IL 2 was dependent on the interaction of IL 2 with the monocytic IL 2 receptor as shown by inhibition experiments with anti IL 2 R monoclonal antibody. Thus the IL 2 driven monocyte/T‐cell interaction leads to an increased Fc‐γ R mediated monocytic respiratory burst activity and to the secretion of a soluble MAF activity, but there w