Krakauer T, Oppenheim J J
Medical Division, USAMRIID, Fort Detrick, Frederick, MD 21702-5011.
J Immunol. 1993 Feb 15;150(4):1205-11.
Stimulation of human blood monocytes (adherent mononuclear cells) and the monocytic 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 II Ag expression by these cells. Both IL-1 and TNF-alpha enhanced the IFN-gamma-induced HLA-DR expression (> twofold) and this effect was inhibited by antibody to IFN-gamma. In the case of human monocytes, IL-1 or TNF-alpha, 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.
白细胞介素-1（IL-1）或肿瘤坏死因子-α（TNF-α）刺激人血单核细胞（贴壁单核细胞）和单核细胞系THP-1，会导致γ干扰素（IFN-γ）受体上调。使用125I-IFN-γ进行的Scatchard分析显示，THP-1细胞上IFN-γ受体的数量增加了两倍，而受体亲和力未发生改变。通过检测IFN-γ对这些细胞上主要组织相容性复合体（MHC）II类抗原表达的影响，研究了单核细胞和THP-1细胞上这种IFN-γ受体诱导的潜在功能意义。IL-1和TNF-α均增强了IFN-γ诱导的人类白细胞抗原-DR（HLA-DR）表达（>两倍），且这种效应被抗IFN-γ抗体抑制。就人单核细胞而言，IL-1或TNF-α单独作用也会增加HLA-DR表达，这同样被抗IFN-γ抗体消除。数据表明，IL-1和TNF-α的免疫增强作用部分是通过增强单核细胞和巨噬细胞上IFN-γ受体的表达来介导的。这可能会增加IFN-γ激活巨噬细胞的能力，使其更有效地表达HLA-DR并呈递抗原。
