Pulmonary innate immunity is required for host defense; however, excessive neutrophil inflammation can cause life-threatening acute lung injury. B lymphocytes can be regulatory, yet little is known about peripheral transitional IgM⁺ B cells in terms of regulatory properties. Using single-cell RNA sequencing, we discovered eight IgM⁺ B cell subsets with unique gene regulatory networks in the lung circulation dominated by transitional type 1 B and type 2 B (T2B) cells. Lung intravital confocal microscopy revealed that T2B cells marginate in the pulmonary capillaries via CD49e and require CXCL13 and CXCR5. During lung inflammation, marginated T2B cells dampened excessive neutrophil vascular inflammation via the specialized proresolving molecule lipoxin A₄ (LXA₄). Exogenous CXCL13 dampened excessive neutrophilic inflammation by increasing marginated B cells, and LXA₄ recapitulated neutrophil regulation in B cell–deficient mice during inflammation and fungal pneumonia. Thus, the lung microvasculature is enriched in multiple IgM⁺ B cell subsets with marginating capillary T2B cells that dampen neutrophil responses.

中文翻译：

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边缘过渡 B 细胞在炎症和肺炎期间调节肺中的中性粒细胞

宿主防御需要肺先天免疫；然而，过度的中性粒细胞炎症会导致危及生命的急性肺损伤。^{B 淋巴细胞可以是调节性的，但就调节特性而言，外周过渡性 IgM +} B 细胞知之甚少。使用单细胞 RNA 测序，我们发现了 8 个 IgM ⁺ B 细胞亚群，在肺循环中具有独特的基因调控网络，主要由过渡型 1 B 和 2 B (T2B) 细胞主导。肺活体共聚焦显微镜显示 T2B 细胞通过 CD49e 在肺毛细血管边缘化，需要 CXCL13 和 CXCR5。_{在肺部炎症期间，边缘化的 T2B 细胞通过专门的分解前分子脂氧素 A 4} ( LXA) 抑制过度的中性粒细胞血管炎症。₄）。外源性 CXCL13 通过增加边缘 B 细胞来抑制过度的中性粒细胞炎症，LXA ₄概括了 B 细胞缺陷小鼠在炎症和真菌性肺炎期间的中性粒细胞调节。因此，肺微脉管系统富含多个 IgM ⁺ B 细胞亚群，具有抑制中性粒细胞反应的边缘毛细血管 T2B 细胞。