CD4+ and CD8+ cells are key participants in the development of recurrent herpetic stromal keratitis in mice
CD4+ and CD8+ cells are key participants in the development of recurrent herpetic stromal keratitis in mice
复制标题
DOI：
10.1006/mpat.2002.0506
复制
发表时间：
2002-06-01
影响因子：
3.8
通讯作者：
Stuart, PM
中科院分区：
文献类型：
--
作者：
Keadle, TL;Morris, JL;Stuart, PM
眼部单纯疱疹病毒（HSV）感染导致免疫介导的角膜基质炎症，称为疱疹性角膜基质炎（HSK）。复发性HSK是人类病毒性角膜盲的常见原因。CD 4（+）和CD 8（+）T细胞亚群在疾病发病机制中的作用尚不明确，并随病毒株和宿主遗传背景而变化。为了研究T细胞亚群对角膜疾病的贡献，我们研究了用HSV-1 McKrae株眼部感染的CD 4或CD 8基因敲除（KO）小鼠中复发性HSK的发展。在UV-B诱导的病毒再激活后，与正常基因型感染的BALB/c小鼠相比，潜伏感染的BALB/c（HSV敏感）CD 4和CD 8 KO小鼠的角膜混浊度降低。相反，C57 BL/6（HSV抗性）CD 4和CD 8 KO潜伏期小鼠的不透明性与遗传正常的潜伏期小鼠没有差异。在C57 BL/6 CD 4/CD 8双KO小鼠中未证实病毒诱导的角膜混浊。通过再活化率、脱落天数或病毒滴度测量，两种品系的CD 4 KO小鼠中均出现病毒脱落增加。我们的研究结果表明，CD 4（+）和CD 8（+）细胞在复发性HSK的免疫发病机制中发挥作用，其作用依赖于宿主的遗传特征。(C)2002爱思唯尔科技有限公司版权所有。
Ocular herpes simplex virus (HSV) infection results in an immune-mediated inflammation of the corneal stroma known as herpetic stromal keratitis (HSK). Recurrent HSK is a common cause of virus-induced corneal blindness in humans. The role of CD4(+) and CD8(+) T cell subsets in the disease pathogenesis is ill defined and varies with the virus strain and host genetic background. To examine the contribution of T cell subsets to corneal disease, we studied the development of recurrent HSK in CD4 or CD8 gene knockout (KO) mice ocularly infected with HSV-1 McKrae strain. Following UV-B induced viral reactivation, corneal opacity in latently infected BALB/c (HSV sensitive) CD4 and CD8 KO mice was reduced compared to infected BALB/c mice with normal genotype. In contrast, opacity in C57BL/6 (HSV resistant) CD4 and CD8 KO latent mice did not differ from genetically normal latent mice. Virus-induced corneal opacity was not demonstrable in C57BL/6 CD4/CD8 double KO mice. Increased viral shedding, measured by reactivation rate, days shedding or viral titers, occurred in CD4 KO mice of both strains. Our findings indicate that both CD4(+) and CD8(+) cells play a role in the immunopathogenesis of recurrent HSK, and their role is dependent upon the host genetic profile. (C) 2002 Elsevier Science Ltd. All rights reserved.