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上皮细胞对 HSV-1 感染的抵抗力依赖于新型先天传感器 IFI-16。

Resistance to HSV-1 infection in the epithelium resides with the novel innate sensor, IFI-16.

机构信息

Department of Microbiology, Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.

出版信息

Mucosal Immunol. 2012 Mar;5(2):173-83. doi: 10.1038/mi.2011.63. Epub 2012 Jan 11.

DOI:10.1038/mi.2011.63
PMID:22236996
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3288395/
Abstract

Toll-like receptors (TLRs) are innate sentinels required for clearance of bacterial and fungal infections of the cornea, but their role in viral immunity is currently unknown. We report that TLR signaling is expendable in herpes simplex virus (HSV)-1 containment as depicted by plaque assays of knockout mice (MyD88(-/-), Trif(-/-) and MyD88(-/-) Trif(-/-) double knockout) resembling wild-type controls. To identify the key sentinel in viral recognition of the cornea, in vivo knockdown of the DNA sensor IFI-16/p204 in the corneal epithelium was performed and resulted in a loss of IFN-regulatory factor-3 (IRF-3) nuclear translocation, interferon-α production, and viral containment. The sensor seems to have a similar function in other HSV clinically relevant sites such as the vaginal mucosa in which a loss of p204/IFI-16 results in significantly more HSV-2 shedding. Thus, we have identified an IRF-3-dependent, IRF-7- and TLR-independent innate sensor responsible for HSV containment at the site of acute infection.

摘要

Toll 样受体 (TLRs) 是清除角膜细菌和真菌感染所必需的先天哨兵，但它们在病毒免疫中的作用目前尚不清楚。我们报告说，TLR 信号在单纯疱疹病毒 (HSV)-1 控制中是可有可无的，这可以通过对类似于野生型对照的敲除小鼠 (MyD88(-/-)、Trif(-/-)和 MyD88(-/-)Trif(-/-)双敲除) 的噬菌斑分析来描绘。为了确定角膜病毒识别中的关键哨兵，在角膜上皮细胞中进行了 DNA 传感器 IFI-16/p204 的体内敲低，导致干扰素调节因子-3 (IRF-3) 核易位、干扰素-α产生和病毒控制的丧失。该传感器在其他与临床相关的 HSV 部位（如阴道黏膜）似乎具有类似的功能，在这些部位，p204/IFI-16 的缺失会导致 HSV-2 的脱落明显增加。因此，我们已经确定了一种 IRF-3 依赖性、IRF-7 和 TLR 非依赖性先天传感器，它负责急性感染部位的 HSV 控制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/a056d7006bef/nihms346676f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/a526800c0ce9/nihms346676f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/f836832359b1/nihms346676f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/60afb48dd13d/nihms346676f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/33108dd6e856/nihms346676f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/39e8c1f5e91c/nihms346676f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/a056d7006bef/nihms346676f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/a526800c0ce9/nihms346676f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/f836832359b1/nihms346676f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/60afb48dd13d/nihms346676f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/33108dd6e856/nihms346676f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/39e8c1f5e91c/nihms346676f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7551/3288395/a056d7006bef/nihms346676f7.jpg

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