Flesch I E, Hess J H, Huang S, Aguet M, Rothe J, Bluethmann H, Kaufmann S H
Department of Immunology, University of Ulm, Germany.
J Exp Med. 1995 May 1;181(5):1615-21. doi: 10.1084/jem.181.5.1615.
Interleukin 12 (IL-12) produced by macrophages immediately after infection is considered essential for activation of a protective immune response against intracellular pathogens. In the murine Mycobacterium bovis Bacillus Calmette-Guérin (BCG) model we assessed whether early IL-12 production by macrophages depends on other cytokines. In vitro, murine bone marrow-derived macrophages produced IL-12 after infection with viable M. bovis BCG or stimulation with LPS, however, priming with recombinant interferon gamma (rIFN-gamma) was necessary. In addition, IL-12 production by these macrophages was blocked by specific anti-tumor necrosis factor alpha (TNF-alpha) antiserum. Macrophages from gene deletion mutant mice lacking either the IFN-gamma receptor or the TNF receptor 1 (p55) failed to produce IL-12 in vitro after stimulation with rIFN-gamma and mycobacterial infection. In vivo, IL-12 production was induced in spleens of immunocompetent mice early during M. bovis BCG infection but not in those of mutant mice lacking the receptors for IFN-gamma or TNF. Our results show that IL-12 production by macrophages in response to mycobacterial infection depends on IFN-gamma and TNF. Hence, IL-12 is not the first cytokine produced in mycobacterial infections.
感染后巨噬细胞立即产生的白细胞介素12(IL-12)被认为是激活针对细胞内病原体的保护性免疫反应所必需的。在小鼠牛分枝杆菌卡介苗(BCG)模型中,我们评估了巨噬细胞早期产生IL-12是否依赖于其他细胞因子。在体外,小鼠骨髓来源的巨噬细胞在用活的牛分枝杆菌卡介苗感染或用脂多糖刺激后产生IL-12,然而,用重组干扰素γ(rIFN-γ)预处理是必要的。此外,这些巨噬细胞产生IL-12的过程被特异性抗肿瘤坏死因子α(TNF-α)抗血清阻断。来自缺乏IFN-γ受体或肿瘤坏死因子受体1(p55)的基因缺失突变小鼠的巨噬细胞,在用rIFN-γ刺激和分枝杆菌感染后,在体外未能产生IL-12。在体内,在牛分枝杆菌卡介苗感染早期,免疫功能正常小鼠的脾脏中可诱导产生IL-12,但在缺乏IFN-γ或TNF受体的突变小鼠脾脏中则不能。我们的结果表明,巨噬细胞对分枝杆菌感染产生IL-12依赖于IFN-γ和TNF。因此,IL-12不是分枝杆菌感染中产生的第一种细胞因子。