【摘要】 目的:探讨结核分枝杆菌对γ-干扰素(IFN-γ)信号转导的作用。方法:体外分离及培养人和鼠类巨噬细胞,感染结核分枝杆菌并收集条件培养基(Mtb-CM);流式细胞仪测定Mtb-CM对人及鼠巨噬细胞的表面标志FcγRI(CD64)和组织相容性Ⅱ类分子(MHCⅡ)的表达。结果:与Mtb-CM共同培养的人巨噬细胞 FcγRI的表达明显低于未加Mtb-CM的对照组(P<0．05);同样,与Mtb—CM共同培养的鼠巨噬细胞MHCⅡ的表达亦明显低于对照组(P<0．05);加入抗IL-6抗体的Mtb—CM可使巨噬细胞对IFN-γ的应答反应提高,其表面标志的表达明显高于未加IL-6抗体的对照组(P<0．05)。结论:结核分枝杆菌诱导巨噬细胞产生的Mtb—CM 可抑制由IFN-γ介导的巨噬细胞表面标志的表达;Mtb—CM中所含的刺激因子可能为IL-6,揭示了IL-6在结核菌感染中的新作用。更多还原

【Abstract】 Objective Objective To study the effect of Mycobacterium tuberculosis (Mtb) on IFN-γ signaling pathway in macrophages. Methods Humans and mice macrophages were isolated and infected by Mtb, condition medium were collected after a few days culture; Macrophage surface expression of FcγRI (human) or MHC II (mouse) was measured by flow cytometry to explore the effect of condition medium on macrophage response to IFN-γ. Results Surface expression of FcγRI in human macrophages cultured in condition medium was significantly decreased compared to those without condition medium (p<0. 05) ; Similarly, surface expression of MHC II in mouse macrophages cultured in the condition medium was significantly decreased compared to those without condition medium (P<0. 05); Condition medium cultured with anti IL-6 antibody improved macrophage response to IFN-γ; Surface expression of MHC II in mouse macrophages cultured in condition medium with anti IL-6 antibody was significantly increased compared to those cultured in condition medium alone (P<0. 05). Conclusion Mtb induced condition medium can inhibit macrophage surface expression of FcγRI or MHC initiated by IFN-γ; At meanwhile, the results also show that IL-6 may play an important role in condition medium which can inhibits macrophage response to IFN-γ, and indicate that IL-6 may have a novel function in the Mtb infection.更多还原