CD4+、CD8+和CD4-CD8-T细胞亚群表达IL-18受体以及响应IL-18产生IFN-γ的差异能力。
Differential capacities of CD4+, CD8+, and CD4-CD8- T cell subsets to express IL-18 receptor and produce IFN-gamma in response to IL-18.
作者信息
Tomura M, Maruo S, Mu J, Zhou X Y, Ahn H J, Hamaoka T, Okamura H, Nakanishi K, Clark S, Kurimoto M, Fujiwara H
机构信息
Biomedical Research Center, Osaka University Medical School, Suita, Japan.
出版信息
J Immunol. 1998 Apr 15;160(8):3759-65.
IL-12 and IL-18 have the capacity to stimulate IFN-gamma production by T cells. Using a T cell clone, we reported that IL-18 responsiveness is generated only after exposure to IL-12. Here, we investigated the induction of IL-18 responsiveness in resting CD8+, CD4+, and CD4-CD8- T cells. Resting T cells respond to neither IL-12 nor IL-18. After stimulation with anti-CD3 plus anti-CD28 mAbs, CD8+, CD4+, and CD4-CD8- T cells expressed IL-12R, but not IL-18R, and produced IFN-gamma in response to IL-12. Cultures of T cells with anti-CD3/anti-CD28 in the presence of rIL-12 induced IL-18R expression and IL-18-stimulated IFN-gamma production, which reached higher levels than that induced by IL-12 stimulation. However, there was a substantial difference in the expression of IL-18R and IL-18-stimulated IFN-gamma production among T cell subsets. CD4+ cells expressed marginal levels of IL-18R and produced small amounts of IFN-gamma, whereas CD8+ cells expressed higher levels of IL-18R and produced more IFN-gamma than CD4+ cells. Moreover, CD4-CD8- cells expressed levels of IL-18R comparable to those for CD8+ cells but produced IFN-gamma one order higher than did CD8+ cells. These results indicate that the induction of IL-18R and IL-18 responsiveness by IL-12 represents a mechanism underlying enhanced IFN-gamma production by resting T cells, but the operation of this mechanism differs depending on the T cell subset stimulated.
白细胞介素-12(IL-12)和白细胞介素-18(IL-18)具有刺激T细胞产生γ干扰素(IFN-γ)的能力。我们利用一个T细胞克隆报道,只有在接触IL-12后,T细胞才会产生对IL-18的反应性。在此,我们研究了静息CD8⁺、CD4⁺和CD4⁻CD8⁻T细胞中IL-18反应性的诱导情况。静息T细胞对IL-12和IL-18均无反应。用抗CD3加抗CD28单克隆抗体刺激后,CD8⁺、CD4⁺和CD4⁻CD8⁻T细胞表达IL-12受体(IL-12R),但不表达IL-18受体(IL-18R),并对IL-12产生IFN-γ。在重组IL-12(rIL-12)存在的情况下,用抗CD3/抗CD28刺激T细胞培养物可诱导IL-18R表达和IL-18刺激的IFN-γ产生,其水平高于IL-12刺激所诱导的水平。然而,T细胞亚群之间在IL-18R表达和IL-18刺激的IFN-γ产生方面存在显著差异。CD4⁺细胞表达的IL-18R水平较低,产生的IFN-γ量较少,而CD8⁺细胞表达的IL-18R水平较高,产生的IFN-γ比CD4⁺细胞更多。此外,CD4⁻CD8⁻细胞表达的IL-18R水平与CD8⁺细胞相当,但产生的IFN-γ比CD错译:原文中“CD4-CD8- cells expressed levels of IL-18R comparable to those for CD8+ cells but produced IFN-gamma one order higher than did CD8+ cells.”的后半句翻译错误,“one order higher”应翻译为“高出一个数量级”,而不是“高出一级”。
正确译文
CD4⁻CD8⁻细胞表达的IL-18R水平与CD8⁺细胞相当,但产生的IFN-γ比CD8⁺细胞高出一个数量级。
8⁺细胞高出一级。这些结果表明,IL-12诱导IL-18R和IL-18反应性是静息T细胞增强IFN-γ产生的一种机制,但该机制的运作因所刺激的T细胞亚群而异。