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首页> 外文期刊>Microbial Pathogenesis >Brucella abortus induces Irgm3 and Irga6 expression via type-I IFN by a MyD88-dependent pathway, without the requirement of TLR2, TLR4, TLR5 and TLR9.
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Brucella abortus induces Irgm3 and Irga6 expression via type-I IFN by a MyD88-dependent pathway, without the requirement of TLR2, TLR4, TLR5 and TLR9.

机译：流产布鲁氏菌通过MyD88依赖性途径通过I型干扰素诱导Irgm3和Irga6表达，而无需TLR2，TLR4，TLR5和TLR9。

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摘要

The innate immune system senses bacterial pathogens by pattern recognition receptors, such as the well-characterised Toll-like Receptors (TLR). The activation of TLR signalling cascades depends on several adaptor proteins, among which MyD88 plays a key role in triggering innate immune responses. Here, we show in murine macrophages that Brucella abortus triggers expression of the interferon-inducible resistance proteins (IRGs, p47 GTPases) via type-I IFN secretion at late time points, when Brucella has reached its replication niche. This induction requires the adaptor molecule MyD88 but does not involve the TLRs normally implicated in sensing Gram-negative bacteria, namely TLR2, TLR4, TLR5 and TLR9. Brucella mutants lacking the functional VirB type-IV secretion system were not capable of inducing Irgm3 and Irga6 expression, suggesting that the type-IV secretion system is part of the triggering of the activation process. Our data suggest that Brucella is recognized intracellularly by an unknown receptor, different from the conventional ones used for Gram-negative sensing, but one that nevertheless signals through MyD88. (C) 2009 Elsevier Ltd. All rights reserved.
机译：先天性免疫系统通过模式识别受体（例如功能强大的Toll样受体（TLR））感知细菌病原体。 TLR信号级联反应的激活取决于几种衔接蛋白，其中MyD88在触发先天免疫应答中起关键作用。在这里，我们在鼠巨噬细胞中显示，流产布鲁氏菌会在晚期布鲁氏菌达到其复制位时通过I型IFN分泌触发干扰素诱导抗性蛋白（IRG，p47 GTPases）的表达。该诱导需要衔接子分子MyD88，但不涉及通常牵涉感测革兰氏阴性细菌的TLR，即TLR2，TLR4，TLR5和TLR9。缺乏功能性VirB IV型分泌系统的布鲁氏菌突变体无法诱导Irgm3和Irga6表达，表明IV型分泌系统是激活过程触发的一部分。我们的数据表明，布鲁氏菌在细胞内被未知受体识别，这与用于革兰氏阴性感测的常规受体不同，但仍然通过MyD88发出信号。 （C）2009 Elsevier Ltd.保留所有权利。

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