Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, United States.
Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, United States; Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, United States.
Virology. 2018 Aug;521:129-137. doi: 10.1016/j.virol.2018.06.002. Epub 2018 Jun 13.
CD8 T cells play a key role in clearance of mouse adenovirus type 1 (MAV-1) from the lung and contribute to virus-induced airway inflammation. We tested the hypothesis that interactions between Fas ligand (FasL) and Fas mediate the antiviral and proinflammatory effects of CD8 T cells. FasL and Fas expression were increased in the lungs of C57BL/6 (B6) mice during MAV-1 respiratory infection. Viral replication and weight loss were similar in B6 and Fas-deficient (lpr) mice. Histological evidence of pulmonary inflammation was similar in B6 and lpr mice, but lung mRNA levels and airway proinflammatory cytokine concentrations were lower in MAV-1-infected lpr mice compared to infected B6 mice. Virus-induced apoptosis in lungs was not affected by Fas deficiency. Our results suggest that the proinflammatory effects of CD8 T cells during MAV-1 infection are mediated in part by Fas activation and are distinct from CD8 T cell antiviral functions.
CD8 T 细胞在清除肺部小鼠腺病毒 1 型（MAV-1）方面发挥关键作用，并有助于病毒引起的气道炎症。我们检验了这样一个假设，即 Fas 配体（FasL）和 Fas 之间的相互作用介导 CD8 T 细胞的抗病毒和促炎作用。在 MAV-1 呼吸道感染期间，C57BL/6（B6）小鼠肺部的 FasL 和 Fas 表达增加。在 B6 和 Fas 缺陷（lpr）小鼠中，病毒复制和体重减轻相似。B6 和 lpr 小鼠的肺部炎症组织学证据相似，但与感染 B6 小鼠相比，感染 MAV-1 的 lpr 小鼠肺部 mRNA 水平和气道促炎细胞因子浓度较低。Fas 缺陷并不影响病毒诱导的肺部细胞凋亡。我们的研究结果表明，CD8 T 细胞在 MAV-1 感染期间的促炎作用部分是通过 Fas 激活介导的，与 CD8 T 细胞抗病毒功能不同。
