Influenza is a deadly and costly infectious disease, even during flu seasons when an effective vaccine has been developed. To improve vaccines against respiratory viruses, a better understanding of the immune response at the site of infection is crucial. After influenza infection, clonally expanded T cells take up permanent residence in the lung, poised to rapidly respond to subsequent infection. Here, we characterized the dynamics and transcriptional regulation of lung-resident CD4⁺ T cells during influenza infection and identified a long-lived, Bcl6-dependent population that we have termed T resident helper (T_RH) cells. T_RH cells arise in the lung independently of lymph node T follicular helper cells but are dependent on B cells, with which they tightly colocalize in inducible bronchus-associated lymphoid tissue (iBALT). Deletion of Bcl6 in CD4⁺ T cells before heterotypic challenge infection resulted in redistribution of CD4⁺ T cells outside of iBALT areas and impaired local antibody production. These results highlight iBALT as a homeostatic niche for T_RH cells and advocate for vaccination strategies that induce T_RH cells in the lung.

流感是一种致命且代价高昂的传染病，即使在开发出有效疫苗的流感季节也是如此。为了改进针对呼吸道病毒的疫苗，更好地了解感染部位的免疫反应至关重要。流感感染后，克隆扩增的 T 细胞在肺中永久驻留，准备对随后的感染迅速作出反应。^{在这里，我们描述了流感感染期间肺驻留 CD4 +} T 细胞的动力学和转录调控，并确定了一个长寿的、依赖Bcl6的群体，我们称之为 T 驻留辅助 (T _RH ) 细胞。相对_湿度细胞独立于淋巴结 T 滤泡辅助细胞在肺中出现，但依赖于 B 细胞，它们与 B 细胞紧密共存于诱导型支气管相关淋巴组织 (iBALT)。在异型攻击感染之前，CD4 + T 细胞中 Bcl6 的缺失导致 CD4 + ^T细胞在^iBALT区域之外重新分布，并损害了局部抗体的产生。这些结果突出了 iBALT 作为 T _RH细胞的稳态生态位，并倡导在肺中诱导 T _{RH细胞的疫苗接种策略。}