首页> 外文期刊>Infection and immunity >MyD88-Deficient Mice Display a Profound Loss in Resistance to Mycobacterium tuberculosis Associated with Partially Impaired Th1 Cytokine and Nitric Oxide Synthase 2 Expression
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MyD88-Deficient Mice Display a Profound Loss in Resistance to Mycobacterium tuberculosis Associated with Partially Impaired Th1 Cytokine and Nitric Oxide Synthase 2 Expression

机译:MyD88缺陷小鼠显示出对部分分枝的Th1细胞因子和一氧化氮合酶2表达受损相关的结核分枝杆菌耐药性的深刻丧失。

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Mycobacterium tuberculosis possesses agonists for several Toll-like receptors (TLRs), yet mice with single TLR deletions are resistant to acute tuberculosis. MyD88?/? mice were used to examine whether TLRs play any role in protection against aerogenic M. tuberculosis H37Rv infection. MyD88?/? mice failed to control mycobacterial replication and rapidly succumbed. Moreover, expressions of interleukin 12, tumor necrosis factor alpha, gamma interferon, and nitric oxide synthase 2 were markedly decreased in the knockout animals. These results argue that resistance to M. tuberculosis must depend on MyD88-dependent signals mediated by an as-yet-undetermined TLR or a combination of TLRs.
机译:结核分枝杆菌对几种Toll样受体(TLR)具有激动剂,但是具有单个TLR缺失的小鼠对急性肺结核具有抗性。使用MyD88 ?/?小鼠检查TLR是否在针对气源性 M的保护中发挥任何作用。结核HemR37感染。 MyD88 ?/?小鼠未能控制分枝杆菌的复制并迅速死亡。此外,基因敲除动物中白介素12,肿瘤坏死因子α,γ干扰素和一氧化氮合酶2的表达明显降低。这些结果表明对 M的抗性。结核病必须依靠尚未确定的TLR或TLR组合介导的MyD88依赖性信号。

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