IL-1 and Tumor Necrosis Factor-Alpha Each Up-Regulate Both the Expression of IFN-Gamma Receptors and Enhance IFN-Gamma-Induced HLA-DR Expression on Human Monocytes and a Human Monocytic Cell Line (THP-1)

摘要

Stimulation of human blood monocytes (adherent mononuclear cells) and themonocytic cell line, THP-1, by IL-1 or TNF-alpha leads to the up-regulation of IFN-gamma receptors. Scatchard analysis using 125I-IFN-gamma revealed a twofold increase in the number of IFN-gamma receptors on THP-1 cells without an alteration in the affinity of the receptor. The potential functional significance of this induction of IFN-gamma receptors on monocytes and THP-1 cells was investigated by examining the effect of IFN-gamma on MHC class 11 Ag expression by these cells. Both IL-1 and TNF-alpha enhanced the IFN-gamma-induced HLA-DR expression (>twofold) an this effect was inhibited by antibody to IFN-gamma. In the case of human monocytes, IL-1 or TNF-A, each by themselves also increased HLA-DR expression, which was also abrogated by antibody to IFN-gamma. The data suggest that the immunopotentiating effects of IL-1 and TNF-alpha are mediated in part by enhancing IFN-gamma receptor expression on monocytes and macrophages. This presumably would increase the capacity of IFN-gamma to activate macrophages, enabling them to express HLA-DR and present Ag more effectively. Journal of Immunology, 1993, 150: 1205.