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首页> 外文期刊>Infection and immunity >Comparison of gamma interferon, tumor necrosis factor, and direct cell contact in activation of antimycobacterial defense in murine macrophages.
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Comparison of gamma interferon, tumor necrosis factor, and direct cell contact in activation of antimycobacterial defense in murine macrophages.

机译：γ干扰素，肿瘤坏死因子和直接细胞接触在小鼠巨噬细胞抗分枝杆菌防御激活中的比较。

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We compared the abilities of gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and sensitized murine lymph node lymphocytes to activate syngeneic murine peritoneal macrophages to inhibit the growth of intracellular Mycobacterium bovis BCG in vitro. IFN-gamma could activate antimycobacterial defense only when added to macrophage cultures prior to their infection with BCG. TNF-alpha was without any effect. In contrast, BCG-sensitized lymphocytes could induce antimycobacterial defenses when added after macrophages had been infected with BCG. The cell-mediated effect required direct contact between effector lymphocytes and the targets (BCG-infected macrophages), as revealed in studies in which these cell populations were separated by a semipermeable membrane. Cyclosporin A, which inhibits the production of relevant macrophage-activating lymphokines, did not abrogate the ability of sensitized lymphocytes to activate antimycobacterial effects in infected macrophages. Furthermore, only BCG-sensitized lymphocytes, and not Listeria-sensitized lymphocytes, could activate the antimycobacterial effects. These lymphocytes were not cytotoxic to the infected macrophages. The presence of anti-TNF-alpha antibody in cocultures reduced the antimicrobial effects. We propose that the activation of antimycobacterial defense in macrophages can occur by direct physical contact with sensitized lymphocytes. This process may be due to lymphocyte membrane-associated TNF-alpha, as we previously demonstrated in our studies of antileishmanial defense.
机译：我们比较了γ干扰素（IFN-γ），肿瘤坏死因子α（TNF-α）和致敏的小鼠淋巴结淋巴细胞激活同系鼠腹膜巨噬细胞以抑制细胞内牛分枝杆菌BCG体外生长的能力。 IFN-γ只有在被BCG感染之前加入巨噬细胞培养物中才能激活抗分枝杆菌防御。 TNF-α没有任何作用。相反，当巨噬细胞已被BCG感染后，添加BCG的淋巴细胞可诱导抗分枝杆菌的防御。细胞介导的作用需要效应子淋巴细胞与靶标（感染了BCG的巨噬细胞）直接接触，正如在研究中揭示的那样，这些细胞群被半透膜隔开。抑制相关巨噬细胞活化淋巴因子产生的环孢菌素A并没有消除致敏淋巴细胞激活被感染巨噬细胞抗分枝杆菌作用的能力。此外，只有BCG敏感的淋巴细胞而不是李斯特菌敏感的淋巴细胞可以激活抗分枝杆菌作用。这些淋巴细胞对感染的巨噬细胞没有细胞毒性。共培养物中抗TNF-α抗体的存在降低了抗微生物作用。我们建议巨噬细胞中抗分枝杆菌防御的激活可以通过与致敏淋巴细胞直接物理接触而发生。如我们先前在抗疟疾防御研究中所证明的，该过程可能是由于淋巴细胞膜相关的TNF-α所致。

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