Immunological dysregulation in asthma is associated with changes in exposure to microorganisms early in life. Gammaherpesviruses (γHVs), such as Epstein-Barr virus, are widespread human viruses that establish lifelong infection and profoundly shape host immunity. Using murid herpesvirus 4 (MuHV-4), a mouse γHV, we show that after infection, lung-resident and recruited group 2 innate lymphoid cells (ILC2s) exhibit a reduced ability to expand and produce type 2 cytokines in response to house dust mites, thereby contributing to protection against asthma. In contrast, MuHV-4 infection triggers GM-CSF production by those lung ILC2s, which orders the differentiation of monocytes (Mos) into alveolar macrophages (AMs) without promoting their type 2 functions. In the context of γHV infection, ILC2s are therefore essential cells within the pulmonary niche that imprint the tissue-specific identity of Mo-derived AMs and shape their function well beyond the initial acute infection.

中文翻译：

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γ 疱疹病毒感染抑制第 2 组先天淋巴样细胞的 2 型特性可重编程肺泡巨噬细胞

哮喘的免疫失调与生命早期接触微生物的变化有关。伽马疱疹病毒 (γHV)，如爱泼斯坦-巴尔病毒，是广泛存在的人类病毒，可建立终生感染并深刻影响宿主免疫力。使用鼠疱疹病毒 4 (MuHV-4)，一种小鼠 γHV，我们表明在感染后，肺驻留和募集的第 2 组先天淋巴样细胞 (ILC2s) 表现出响应屋尘螨而扩增和产生 2 型细胞因子的能力降低，从而有助于预防哮喘。相反，MuHV-4 感染会触发那些肺部 ILC2 产生 GM-CSF，从而命令单核细胞 (Mos) 分化为肺泡巨噬细胞 (AM)，而不促进其 2 型功能。在γHV感染的情况下，