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Innate sensing of bacterial cyclic dinucleotides: More than just STING

机译:细菌环状二核苷酸的先天感知:不仅仅是STING

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The detection of viral and bacterial nucleic acids by the innate immune system, which leads to the induction of type I interferons (IFN-alpha and IFN-beta), is now an area of intense research. The interest is not only in determining the mechanisms whereby pathogens are sensed but also in understanding how inappropriate activation of such mechanisms by self nucleic acids can lead to autoimmunity. Host pattern-recognition receptors (PRRs) that detect pathogen RNA and DNA on the cell surface, in endosomes and within the cytosol and nucleus have been proposed and identified and, in some cases (such as the Toll-like receptors) characterized extensively. However, it has become apparent that small bacterial nucleic acids called 'cyclic dinucleo-tides' (CDNs) are also able to elicit an innate immune response when present in the cytosol. In a study published in this issue of Nature Immunology, Parvatiyar et al. show that the cellular DEAD (aspartate-glutamate-alanine-aspartate)-box helicase DDX41 binds bacterial CDNs and is responsible for activating the signaling pathway that leads to the induction of type I interferons.
机译:通过先天免疫系统对病毒和细菌核酸的检测,导致诱导I型干扰素(IFN-α和IFN-β),现已成为一个研究热点。兴趣不仅在于确定感测病原体的机制,而且在于理解自身核酸对此类机制的不适当激活如何导致自身免疫。已经提出并鉴定了检测细胞表面,内体中以及细胞质和细胞核内的病原体RNA和DNA的宿主模式识别受体(PRR),并且在某些情况下(例如Toll样受体)具有广泛的特征。但是,很明显的是,被称为“环二核苷酸”(CDN)的小型细菌核酸也可以在细胞质中存在时引发先天性免疫应答。在本期《自然免疫学》上发表的一项研究中,Parvatiyar等人。表明细胞DEAD(天冬氨酸-谷氨酸-丙氨酸-天冬氨酸)盒解旋酶DDX41结合细菌CDN,并负责激活导致诱导I型干扰素的信号传导途径。

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