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首页> 外文期刊>Nature immunology >Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β
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Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β

机译：一氧化氮通过抑制NLRP3炎性体依赖性IL-1β的加工来控制结核的免疫病理

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摘要

Interleukin 1 (IL-1) is an important mediator of innate immunity but can also promote inflammatory tissue damage. During chronic infections such as tuberculosis, the beneficial antimicrobial role of IL-1 must be balanced with the need to prevent immunopathology. By exogenously controlling the replication of Mycobacterium tuberculosis in vivo, we obviated the requirement for antimicrobial immunity and discovered that both IL-1 production and infection-induced immunopathology were suppressed by lymphocyte-derived interferon-γ (IFN-γ). This effect was mediated by nitric oxide (NO), which we found specifically inhibited assembly of the NLRP3 inflammasome via thiol nitrosylation. Our data indicate that the NO produced as a result of adaptive immunity is indispensable in modulating the destructive innate inflammatory responses elicited during persistent infections.
机译：白介素1（IL-1）是先天免疫的重要介体，但也可以促进炎性组织损伤。在诸如结核病的慢性感染中，IL-1的有益抗菌作用必须与预防免疫病理的需求相平衡。通过在体内外源控制结核分枝杆菌的复制，我们消除了对抗菌素免疫的要求，并发现淋巴细胞衍生的干扰素-γ（IFN-γ）抑制了IL-1的产生和感染诱导的免疫病理。一氧化氮（NO）介导了这种作用，我们发现它通过硫醇亚硝化作用特异性抑制了NLRP3炎性小体的组装。我们的数据表明，由于适应性免疫而产生的NO在调节持续性感染期间引起的破坏性先天性炎症反应中必不可少。

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