抑制 I 型干扰素信号转导以避免细胞内在的宿主细胞防御。
inhibits type I interferon signaling to avoid cell-intrinsic host cell defense.
机构信息
Department of Cell Biology and Molecular Genetics, University of Maryland , College Park, Maryland, USA.
Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, Maryland, USA.
出版信息
Infect Immun. 2023 Nov 16;91(11):e0036523. doi: 10.1128/iai.00365-23. Epub 2023 Oct 16.
The host type I interferon (IFN) response protects against infections. Other bacterial pathogens inhibit type I IFN-mediated cell signaling; however, the interaction between this signaling pathway and has not been well described. Here, we demonstrate that inhibits the IFN-β signaling pathway but does not inhibit IFN-γ-mediated cell signaling. The addition of IFN-β to -infected macrophages limited bacterial growth independently of NOS2 and reactive nitrogen species. The type IV secretion system of is required to inhibit IFN-β-mediated cell signaling. Finally, we show that the inhibition of the IFN-β signaling pathway occurs downstream of STAT1 and STAT2 phosphorylation. In conclusion, our findings describe a novel host cell signaling pathway inhibited by via its type IV secretion system.
宿主 I 型干扰素(IFN)反应可预防感染。其他细菌病原体抑制 I 型 IFN 介导的细胞信号转导;然而,该信号通路与的相互作用尚未得到很好的描述。在这里,我们证明了抑制 IFN-β信号通路,但不抑制 IFN-γ介导的细胞信号转导。IFN-β的添加到感染的巨噬细胞中独立于 NOS2 和活性氮物种限制了细菌的生长。的 IV 型分泌系统是抑制 IFN-β介导的细胞信号转导所必需的。最后,我们表明 IFN-β信号通路的抑制发生在 STAT1 和 STAT2 磷酸化的下游。总之,我们的发现描述了一种新的宿主细胞信号通路,该通路被其 IV 型分泌系统抑制。