A functional type I interferon pathway drives resistance to cornea herpes simplex virus type 1 infection by recruitment of leukocytes

被引：37

作者：

Conrady, Christopher D. ^{[1
]}

Jones, Heather ^{[1
]}

Zheng, Min ^{[2
]}

Carr, Daniel J. J. ^{[1
,2
]}

机构：

[1] Univ Oklahoma, Hlth Sci Ctr, Dept Immunol Microbiol, Oklahoma City, OK 73104 USA

[2] Univ Oklahoma, Hlth Sci Ctr, Dept Ophthalmol, Oklahoma City, OK 73104 USA

来源：

JOURNAL OF BIOMEDICAL RESEARCH | 2011年 / 25卷 / 02期

关键词：

herpes simplex virus type 1; type I interferon; cornea; viral infection; leukocytes; ocular immunology;

D O I：

10.1016/S1674-8301(11)60014-6

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Type I interferons are critical antiviral cytokines produced following herpes simplex virus type-1 (HSV-1) infection that act to inhibit viral spread. In the present study, we identify HSV-infected and adjacent uninfected corneal epithelial cells as the source of interferon-alpha. We also report mice deficient in the A1 chain of the type I IFN receptor (CD118(-/-)) are extremely sensitive to ocular infection with low doses (100 PFU) of HSV-1 as seen by significantly elevated viral titers in the cornea compared to wild type (WT) controls. The enhanced susceptibility correlated with a loss of CD4(+) and CD8(+) T cell recruitment and aberrant chemokine production in the cornea despite mounting an adaptive immune response in the draining mandibular lymph node of CD118-/- mice. Taken together, these results highlight the importance of IFN production in both the innate immune response as well as eliciting chemokine production required to facilitate adaptive immune cell trafficking.

引用

页码：111 / 119

页数：9

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