CD8 T cells are key components of the immune response to viruses, but their roles in the pathogenesis of adenovirus respiratory infection have not been characterized. We used mouse adenovirus type 1 (MAV-1) to define CD8 T cell contributions to the pathogenesis of adenovirus respiratory infection. CD8 T cell deficiency in β2m-/- mice had no effect on peak viral replication in lungs, but clearance of virus was delayed in β2m-/- mice. Virus-induced weight loss and increases in bronchoalveolar lavage fluid total protein, IFN-γ, TNF-α, IL-10, CCL2, and CCL5 concentrations were less in β2m-/- mice than in controls. CD8 T cell depletion had similar effects on virus clearance, weight loss, and inflammation. Deficiency of IFN-γ or perforin had no effect on viral replication or inflammation, but perforin-deficient mice were partially protected from weight loss. CD8 T cells promote MAV-1-induced pulmonary inflammation via a mechanism that is independent of direct antiviral effects.

中文翻译：

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CD8 T细胞对小鼠1型腺病毒呼吸道感染的发病机制的贡献。

CD8 T细胞是对病毒免疫反应的关键组成部分，但其在腺病毒呼吸道感染的发病机理中的作用尚未确定。我们使用1型小鼠腺病毒（MAV-1）定义CD8 T细胞对腺病毒呼吸道感染的发病机制的贡献。β2m-/-小鼠的CD8 T细胞缺乏对肺部病毒复制峰值没有影响，但β2m-/-小鼠的病毒清除被延迟。与对照组相比，β2m-/-小鼠中病毒引起的体重减轻和支气管肺泡灌洗液总蛋白，IFN-γ，TNF-α，IL-10，CCL2和CCL5浓度的增加要少。CD8 T细胞耗竭对病毒清除，体重减轻和炎症有相似的影响。缺乏IFN-γ或穿孔素对病毒复制或炎症没有影响，但缺乏穿孔素的小鼠受到部分保护，免受体重减轻。CD8 T细胞通过独立于直接抗病毒作用的机制促进MAV-1诱导的肺部炎症。