IFI204在感染过程中IFN-β释放和自噬激活中的核心作用。

Chunfa Liu, Xin Sun, Qiang Li, Sreevatsan Srinand, Yang Lifeng, Zhao Deming, Zhou Xiangmei

State Key Laboratories for Agrobiotechnology, Key Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural UniversityBeijing, China.

Department of Veterinary Medicine, College of Agriculture, Ningxia UniversityYinchuan, China.

Front Cell Infect Microbiol. 2017 May 5;7:169. doi: 10.3389/fcimb.2017.00169. eCollection 2017.

() is the pathogen of animals and humans that can replicate in the phagosomes of myeloid cells. Cytosolic detection of bacterial products plays a crucial role in initiating the innate immune response, including autophagy activation and interferon-β (IFN-β) release. Although IFN-β release and autophagy activation have been reported during mycobacterium infection, the mechanisms underlying remains poorly defined. Here, we demonstrated that IFN-β release increases in macrophages exposed to and this requires the activation of the DNA sensor of interferon-γ inducible protein 204 (IFI204). Knockdown of the IFI204 in immortalized and primary murine macrophages blocked IFN-β production and autophagy marker LC3 expression. Thus, our results indicate that the IFI204 is an important sensor for innate immune responses of infection.

（）是可在髓样细胞吞噬体中复制的动物和人类病原体。细菌产物的胞质检测在启动先天免疫反应中起关键作用，包括自噬激活和干扰素-β（IFN-β）释放。尽管在分枝杆菌感染期间已报道了IFN-β释放和自噬激活，但其潜在机制仍不清楚。在这里，我们证明暴露于的巨噬细胞中IFN-β释放增加，这需要激活干扰素-γ诱导蛋白204（IFI204）的DNA传感器。在永生化和原代小鼠巨噬细胞中敲低IFI204可阻断IFN-β产生和自噬标志物LC3表达。因此，我们的结果表明IFI204是感染先天免疫反应的重要传感器。