Resistance to HSV-1 infection in the epithelium resides with the novel innate sensor, IFI-16.
Resistance to HSV-1 infection in the epithelium resides with the novel innate sensor, IFI-16.
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作者：
Toll样受体（TLR）是清除角膜细菌和真菌感染所需的先天性哨兵，但其在病毒免疫中的作用目前尚不清楚。我们报告TLR信号在HSV-1遏制中是消耗性的，如敲除小鼠（MyD 88 −/−，Trif−/−和MyD 88 −/− Trif−/− DKO）类似于野生型对照的空斑试验所示。为了鉴定角膜病毒识别中的关键前哨，进行了角膜上皮中DNA传感器IFI-16/p204的体内敲除，导致IRF-3核转位、干扰素-α产生和病毒遏制的丧失。该传感器似乎在其他HSV临床相关部位（例如阴道粘膜）中具有类似的功能，其中p204/IFI-16的缺失导致显著更多的HSV-2脱落。因此，我们已经鉴定了一种IRF-3依赖性、IRF-7和TLR非依赖性的先天感受器，其负责在急性感染部位的HSV遏制。
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 TLR signaling is expendable in HSV-1 containment as depicted by plaque assays of knockout mice (MyD88−/−, Trif−/− and MyD88−/− Trif−/− DKO) 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 corneal epithelium was performed and resulted in a loss of IRF-3 nuclear translocation, interferon-α production, and viral containment. The sensor appears 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.
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影响因子：
5.4
作者：
Conrady, Christopher D.;Halford, William P.;Carr, Daniel J. J.
通讯作者：
Carr, Daniel J. J.
DOI：
10.1084/jem.189.4.663
发表时间：
1999-02-15
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Leib DA;Harrison TE;Laslo KM;Machalek MA;Moorman NJ;Virgin HW
通讯作者：
Virgin HW
影响因子：
4.4
作者：
Conrady, Christopher D.;Thapa, Manoj;Carr, Daniel J. J.
通讯作者：
Carr, Daniel J. J.
影响因子：
4.4
作者：
Garvey, TL;Dyer, KD;Rosenberg, HF
通讯作者：
Rosenberg, HF
影响因子：
4.4
作者：
Al-Khatib, K;Williams, BRG;Carr, DJJ
通讯作者：
Carr, DJJ