A functional type Ⅰ interferon pathway drives resistance to cornea herpes simplex virus type 1 infection by recruitment of leukocytes
Christopher D. Conrady
Heather Jones
Min Zheng
Daniel J.J. Carr
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-α. We also report mice deficient in the Al chain of the type Ⅰ IFN receptor (CDll8<'-/->) 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 susceptibil-ity 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.
机标关键词：wild typeimmune responsecorneal epithelial cellsherpes simplex viruschemokineTypeimmune celllymph node
分类号：R772.21(眼纤维膜疾病)
资助基金：This work was supported by USPHS grant(AI053108)Daniel JJ.Carr.Additional support includes P20(RR0l7703)an unrestricted grant from Research to Prevent Blindness.Daniel J.J.Carr.is an OUHSC Presbyterian Health Foundation Presidential Professor recipient.Prof.Christopher D.Conrady is supported by NIAID training grant(AI007633)
论文发表日期：2011-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
英文信息