In humans and mice, mucosal immune responses are dominated by IgA antibodies and the cytokine TGF‐β, suppressing unwanted immune reactions but also targeting Ig class switching to IgA. It had been suggested that eosinophils promote the generation and maintenance of mucosal IgA‐expressing plasma cells. Here, we demonstrate that not eosinophils, but specific bacteria determine mucosal IgA production. Co‐housing of eosinophil‐deficient mice with mice having high intestinal IgA levels, as well as the intentional microbiota transfer induces TGF‐β expression in intestinal T follicular helper cells, thereby promoting IgA class switching in Peyer's patches, enhancing IgA⁺ plasma cell numbers in the small intestinal lamina propria and levels of mucosal IgA. We show that bacteria highly enriched for the genus Anaeroplasma are sufficient to induce these changes and enhance IgA levels when adoptively transferred. Thus, specific members of the intestinal microbiota and not the microbiota as such regulate gut homeostasis, by promoting the expression of immune‐regulatory TGF‐β and of mucosal IgA.

中文翻译：

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特定的微生物群通过诱导小鼠Peyer斑块的T滤泡辅助细胞中的TGF-β来增强肠道IgA水平。

在人和小鼠中，粘膜免疫反应受IgA抗体和细胞因子TGF-β的支配，不仅抑制了有害的免疫反应，而且还针对将Ig类转换为IgA。有人提出，嗜酸性粒细胞可促进粘膜表达IgA浆细胞的生成和维持。在这里，我们证明不是嗜酸性粒细胞，而是特定细菌决定粘膜IgA的产生。嗜酸性粒细胞缺乏的小鼠与高肠IgA水平的小鼠以及有意的微生物群转移的共居可诱导T肠小卵泡辅助细胞中TGF-β的表达，从而促进Peyer斑块中IgA类的转换，从而提高IgA ⁺浆细胞的数量在小肠固有层和粘膜IgA水平。我们表明细菌高度丰富的属当过继转移时，厌氧菌足以诱导这些变化并提高IgA水平。因此，肠道菌群的特定成员而非肠道菌群的特定成员通过促进免疫调节性TGF-β和粘膜IgA的表达来调节肠道稳态。