Gessl A, Willheim M, Spittler A, Agis H, Krugluger W, Boltz-Nitulescu G
Institute of General and Experimental Pathology, University of Vienna, Austria.
Scand J Immunol. 1994 Feb;39(2):151-6. doi: 10.1111/j.1365-3083.1994.tb03354.x.
The expression of Fc receptors for IgG (Fc gamma R) and IgA (Fc alpha R) and of various other antigens on the human monocytic cell line U937 and peripheral blood monocytes, under stimulation with human recombinant tumour necrosis factor-alpha (TNF-alpha) and other cytokines, was investigated by flow cytometry. TNF-alpha, as well as interferon-gamma (IFN-gamma) or interleukin-6 (IL-6) had a significant up-regulating effect on U937 expression of Fc gamma RI/CD64. Furthermore, the action of TNF-alpha was augmented by IL-6, and more evidently by IFN-gamma. IFN-alpha alone had only a marginal effect, but was able to increase the TNF-alpha-driven Fc gamma RI expression. In contrast to U937 cells, TNF-alpha did not enhance significantly Fc gamma RI expression on human monocytes. Interestingly, on both U937 cells and monocytes, Fc alpha R was augmented markedly by TNF-alpha. Furthermore, TNF-alpha induced the expression of HLA-DR and HLA-DP antigens on monocytes and U937 cells. The expression of Fc gamma RII/CD32, FC gamma RIII/CD16, CD14, complement receptor type 1 (CR1/CD35), CR4 (CD11c/CD18), and MHC class-I antigens, was not influenced significantly by TNF-alpha. The results of this study show that TNF-alpha may act on human mononuclear phagocytes, alone or in combination with other cytokines, by modulating the expression of various cell-surface antigens.
采用流式细胞术研究了在人重组肿瘤坏死因子-α(TNF-α)和其他细胞因子刺激下,人单核细胞系U937和外周血单核细胞上IgG的Fc受体(FcγR)、IgA的Fc受体(FcαR)以及各种其他抗原的表达情况。TNF-α以及干扰素-γ(IFN-γ)或白细胞介素-6(IL-6)对U937细胞FcγRI/CD64的表达具有显著的上调作用。此外,IL-6增强了TNF-α的作用,IFN-γ的增强作用更明显。单独的IFN-α只有轻微作用,但能够增加TNF-α驱动的FcγRI表达。与U937细胞不同,TNF-α并未显著增强人单核细胞上FcγRI的表达。有趣的是,在U937细胞和单核细胞上,TNF-α均显著增加了FcαR的表达。此外,TNF-α诱导了单核细胞和U937细胞上HLA-DR和HLA-DP抗原的表达。FcγRII/CD32、FcγRIII/CD16、CD14、1型补体受体(CR1/CD35)、CR4(CD11c/CD18)和MHC I类抗原的表达未受到TNF-α的显著影响。本研究结果表明,TNF-α可能通过调节各种细胞表面抗原的表达,单独或与其他细胞因子联合作用于人单核吞噬细胞。