An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection.
An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection.
复制标题
干扰素伽马在抗性结核病感染中的重要作用。
DOI：
10.1084/jem.178.6.2249
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发表时间：
1993-12-01
影响因子：
15.3
通讯作者：
Bloom, B R
中科院分区：
文献类型：
--
作者：
Flynn, J L;Chan, J;Triebold, K J;Dalton, D K;Stewart, T A;Bloom, B R
结核病是发展中国家的一个主要健康问题，近年来在许多工业化国家重新出现。免疫功能低下的个体对结核病的易感性增加，许多实验研究表明T细胞介导的免疫在耐药中起重要作用。淋巴因子干扰素γ（IFN-γ）被认为是巨噬细胞活化和抵抗细胞内病原体的主要介质。由于IFN-γ基因的靶向破坏，已经开发出不能产生IFN-γ（gko）的小鼠。感染结核杆菌后，尽管gko小鼠会出现肉芽肿，但它们无法产生活性氮中间产物，也无法限制杆菌的生长。与对照小鼠相比，gko小鼠表现出组织坏死增加，并死于快速和致命的结核病过程，其可以通过用外源性重组IFN-γ治疗来延迟，但不能预防。
Tuberculosis, a major health problem in developing countries, has reemerged in recent years in many industrialized countries. The increased susceptibility of immunocompromised individuals to tuberculosis, and many experimental studies indicate that T cell- mediated immunity plays an important role in resistance. The lymphokine interferon gamma (IFN-gamma) is thought to be a principal mediator of macrophage activation and resistance to intracellular pathogens. Mice have been developed which fail to produce IFN-gamma (gko), because of a targeted disruption of the gene for IFN-gamma. Upon infection with Mycobacterium tuberculosis, although they develop granulomas, gko mice fail to produce reactive nitrogen intermediates and are unable to restrict the growth of the bacilli. In contrast to control mice, gko mice exhibit heightened tissue necrosis and succumb to a rapid and fatal course of tuberculosis that could be delayed, but not prevented, by treatment with exogenous recombinant IFN-gamma.