Pulmonary immunity requires tight regulation, as interstitial inflammation can compromise gas exchange and lead to respiratory failure. Here we found a greater number of aged CD11b^hiL-selectin^loCXCR4⁺ polymorphonuclear leukocytes (PMNs) in lung vasculature than in the peripheral circulation. Using pulmonary intravital microscopy, we observed lung PMNs physically interacting with B cells via β₂ integrins; this initiated neutrophil apoptosis, which led to macrophage-mediated clearance. Genetic deletion of B cells led to the accumulation of aged PMNs in the lungs without systemic inflammation, which caused pathological fibrotic interstitial lung disease that was attenuated by the adoptive transfer of B cells or depletion of PMNs. Thus, the lungs are an intermediary niche in the PMN lifecycle wherein aged PMNs are regulated by B cells, which restrains their potential to cause pulmonary pathology.

中文翻译：

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在缺乏B细胞调节的情况下，老化的多形核白细胞会引起纤维化间质性肺疾病。

肺免疫需要严格的调节，因为间质性炎症会损害气体交换并导致呼吸衰竭。在这里，我们发现了更大数目的老化细胞CD11b^喜L-选择^LO CXCR4 ⁺多形核白细胞（PMN）在肺脉管系统比外周循环。使用肺活体显微镜，我们观察到肺的PMN物理经由β与B细胞相互作用₂整合素; 这开始中性粒细胞凋亡，从而导致巨噬细胞介导的清除。B细胞的遗传缺失导致衰老的PMN在肺中积累，而没有全身性炎症，从而导致病理性纤维化间质性肺病，这种疾病通过B细胞的过继转移或PMN的消耗而减弱。因此，肺是PMN生命周期中的中间生态位，其中老化的PMN受B细胞调节，从而限制了其引起肺病理的潜力。