The Gram‐negative bacterial pathogen Yersinia delivers six effector proteins into the host cells to block the host innate immune response. One of the effectors, YopT, is a potent cysteine protease that causes the disruption of the actin cytoskeleton to inhibit phagocytosis of the pathogen; however, its molecular mechanism and relevance to pathogenesis need further investigation. In this report, we show that RIG‐I is a novel target of the YopT protein. Remarkably, YopT interacts with RIG‐I and inhibits rat liver homogenate‐mediated nuclear factor‐κB and interferon regulatory factor‐3 activation. Further studies revealed a YopT‐dependent increase in the K48‐polymerized ubiquitination of RIG‐I. These findings suggest that YopT negatively regulates RIG‐I‐mediated cellular antibacterial response by targeting RIG‐I.

中文翻译：

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耶尔森氏菌YopT抑制RLH介导的NF-κB和IRF3信号转导。

革兰氏阴性细菌病原体耶尔森氏菌将六种效应蛋白送入宿主细胞，以阻断宿主的先天免疫反应。效应子之一，YopT，是一种有效的半胱氨酸蛋白酶，可引起肌动蛋白细胞骨架的破坏，从而抑制病原体的吞噬作用。但是，其分子机制及其与发病机制的关系尚需进一步研究。在本报告中，我们表明RIG-I是YopT蛋白的新型靶标。值得注意的是，YopT与RIG-I相互作用并抑制大鼠肝匀浆介导的核因子κB和干扰素调节因子3的活化。进一步的研究表明，RIG-1的K48聚合泛素化具有YopT依赖性增加。这些发现表明，YopT通过靶向RIG-I负调节RIG-I介导的细胞抗菌反应。