Yoshihara R, Shiozawa S, Fujita T, Chihara K
Department of Medicine, Kobe University School of Medicine, Japan.
Infect Immun. 1993 Aug;61(8):3117-22. doi: 10.1128/iai.61.8.3117-3122.1993.
Gamma interferon (IFN-gamma) production from cultured human peripheral blood mononuclear cells was studied during stimulation with Staphylococcus aureus Cowan I or S. aureus Wood. IFN-gamma was specifically produced from CD16+ natural killer (NK) cells under stimulation by S. aureus Cowan I or Wood because these strains (i) induced IFN-gamma production exclusively from CD3-, CD4- CD8-, and CD16+ cells and (ii) induced CD69 and interleukin 2 (IL-2) receptor alpha expression on CD16+ cells without simultaneously augmenting CD71 or IL-2 receptor alpha on T cells. The effects of biological agents on the induction of S. aureus-induced IFN-gamma production paralleled those of S. aureus-induced CD69 expression on CD16+ cells: IL-2, IFN-alpha, and indomethacin augmented the S. aureus-induced IFN-gamma production, whereas IL-4, transforming growth factor beta 1, prostaglandin E2, and dexamethasone inhibited it. However, IFN-alpha was unique in that it did not induce IFN-gamma production from NK cells while it simultaneously augmented CD69 expression on NK cells, suggesting a unique pathway in the activation of NK cells. Thus, we may conclude that S. aureus-induced IFN-gamma production appears to faithfully represent NK cell function within peripheral blood mononuclear cells.
研究了在金黄色葡萄球菌考恩I株或金黄色葡萄球菌伍德株刺激培养的人外周血单个核细胞期间γ干扰素(IFN-γ)的产生情况。IFN-γ是在金黄色葡萄球菌考恩I株或伍德株刺激下由CD16⁺自然杀伤(NK)细胞特异性产生的,因为这些菌株(i)仅诱导CD3⁻、CD4⁻、CD8⁻和CD16⁺细胞产生IFN-γ,并且(ii)诱导CD16⁺细胞上CD69和白细胞介素2(IL-2)受体α表达,而不同时增加T细胞上的CD71或IL-2受体α表达。生物制剂对金黄色葡萄球菌诱导的IFN-γ产生的诱导作用与金黄色葡萄球菌诱导的CD16⁺细胞上CD69表达的诱导作用相似:IL-2、IFN-α和吲哚美辛增强金黄色葡萄球菌诱导的IFN-γ产生,而IL-4、转化生长因子β1、前列腺素E2和地塞米松则抑制该产生。然而,IFN-α的独特之处在于它不会诱导NK细胞产生IFN-γ,同时却会增加NK细胞上的CD69表达,这表明NK细胞激活存在独特途径。因此,我们可以得出结论,金黄色葡萄球菌诱导的IFN-γ产生似乎忠实地反映了外周血单个核细胞内NK细胞的功能。