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Bacteria tune interferon responses by playing with chromatin

机译:细菌通过染色质来调节干扰素反应

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Bacterial infections, like their viral counterparts, trigger the onset of innate immune defense mechanisms through the release of cytokines, including interferons (IFNs). While type I and II IFN responses to bacteria have long been explored, type III IFN response remains poorly addressed. We have recently reported that the pathogen Listeria monocytogenes triggers the expression of type I and III IFN genes in epithelial cells, and is able to fine-tune downstream signaling at the chromatin level. This bacterium can negatively or positively modulate the expression of interferon-stimulated genes (ISGs) by manipulating the function of BAHD1, a component of a host chromatin-silencing complex. To this end, L. monocytogenes tightly controls the secretion of a BAHD1 inhibitory factor, LntA. Here, we further document the current knowledge about chromatin mechanisms modulating interferon responses during host-bacteria interplay, and discuss their physiological consequences.
机译:细菌感染与病毒感染一样,通过释放包括干扰素(IFN)在内的细胞因子来触发先天性免疫防御机制的发作。虽然对细菌的I型和II型IFN应答已进行了很长的研究,但III型IFN的应答仍然难以解决。最近,我们报道了病原性单核细胞增生性李斯特菌触发上皮细胞中I型和III型IFN基因的表达,并能够在染色质水平上微调下游信号。该细菌可以通过操纵宿主染色质沉默复合物的成分BAHD1的功能来负向或正向调节干扰素刺激基因(ISG)的表达。为此,单核细胞增生李斯特菌严格控制BAHD1抑制因子LntA的分泌。在这里,我们进一步记录有关染色质机制调控宿主细菌相互作用过程中干扰素反应的当前知识,并讨论它们的生理后果。

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