B lymphocytes are among the cell types whose effector functions are modulated by mast cells (MCs). The B/MC crosstalk emerged in several pathological settings, notably the colon of inflammatory bowel disease (IBD) patients is a privileged site in which MCs and IgA⁺ cells physically interact. Herein, by inducing conditional depletion of MCs in red MC and basophil (RMB) mice, we show that MCs control B cell distribution in the gut and IgA serum levels. Moreover, in dextran sulfate sodium (DSS)‐treated RMB mice, the presence of MCs is fundamental for the enlargement of the IgA⁺ population in the bowel and the increase of systemic IgA production. Since both conventional B‐2 and peritoneal‐derived B cells populate the intestine and communicate with MCs in physiological conditions and during inflammation, we further explored this interplay through the use of co‐cultures. We show that MCs finely regulate different aspects of splenic B cell biology while peritoneal B cells are unresponsive to the supporting effects provided by MCs. Interestingly, peritoneal B cells induce a pro‐inflammatory skewing in MCs, characterized by increased ST2 and TNF‐α expression. Altogether, this study uncovers the versatility of the B/MC liaison and highlights key aspects for the resolution of intestinal inflammation.

中文翻译：

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肥大细胞与肠道中的B细胞发生串扰并在发炎的肠道中维持IgA反应

B淋巴细胞是其效应功能受肥大细胞（MCs）调节的细胞类型之一。B / MC串扰出现在几种病理情况下，特别是炎症性肠病（IBD）患者的结肠是MC和IgA ⁺细胞物理相互作用的特权部位。在本文中，通过在红色MC和嗜碱性粒细胞（RMB）小鼠中诱导MC的条件耗竭，我们显示MC控制了肠道和IgA血清中B细胞的分布。此外，在用葡聚糖硫酸钠（DSS）处理的人民币小鼠中，MC的存在对于IgA ⁺的增大至关重要肠内细菌数量增加和全身IgA产生增加。由于常规的B-2和腹膜来源的B细胞都在肠道中分布并在生理条件下和炎症过程中与MC通讯，因此我们通过使用共培养物进一步探讨了这种相互作用。我们显示MC很好地调节脾脏B细胞生物学的不同方面，而腹膜B细胞对MC提供的支持作用无反应。有趣的是，腹膜B细胞可诱导MC的促炎性倾斜，其特征是ST2和TNF-α表达增加。总之，这项研究揭示了B / MC联络的多功能性，并强调了解决肠道炎症的关键方面。