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首页> 外文期刊>Cell metabolism >Gut Microbiota-Stimulated Innate Lymphoid Cells Support beta-Defensin 14 Expression in Pancreatic Endocrine Cells, Preventing Autoimmune Diabetes
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Gut Microbiota-Stimulated Innate Lymphoid Cells Support beta-Defensin 14 Expression in Pancreatic Endocrine Cells, Preventing Autoimmune Diabetes

机译：肠道微生物肿块刺激的先天淋巴细胞支持β-defensin 14在胰腺内分泌细胞中表达，预防自身免疫性糖尿病

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摘要

The gut microbiota is essential for the normal function of the gut immune system, and microbiota alterations are associated with autoimmune disorders. However, how the gut microbiota prevents autoimmunity in distant organs remains poorly defined. Here we reveal that gut microbiota conditioned innate lymphoid cells (ILCs) induce the expression of mouse beta-defensin 14 (mBD14) by pancreatic endocrine cells, preventing autoimmune diabetes in the non-obese diabetic (NOD) mice. MBD14 stimulates, via Toll-like receptor 2, interleukin-4 (IL-4)-secreting B cells that induce regulatory macrophages, which in turn induce protective regulatory T cells. The gut microbiota-derived molecules, aryl hydrocarbon receptor (AHR) ligands and butyrate, promote IL-22 secretion by pancreatic ILCs, which induce expression of mBD14 by endocrine cells. Dysbiotic microbiota and low-affinity AHR allele explain the defective pancreatic expression of mBD14 observed in NOD mice. Our study reveals a yet unidentified crosstalk between ILCs and endocrine cells in the pancreas that is essential for the prevention of autoimmune diabetes development.
机译：肠道微生物生物对于肠道免疫系统的正常功能至关重要，并且微生物消毒剂改变与自身免疫障碍有关。但是，肠道微生物群如何防止遥远器官的自身免疫仍然定义不足。在这里，我们揭示了肠道微生物群调节先天淋巴细胞（ILCs）通过胰腺内分泌细胞诱导小鼠β-防御素14（MBD14）的表达，预防非肥胖糖尿病（NOD）小鼠中的自身免疫性糖尿病。 MBD14通过Toll样受体2刺激白细胞介素-4（IL-4） - 诱导调节巨噬细胞的分泌B细胞，这反过来诱导保护性调节性T细胞。肠道微生物A衍生的分子，芳基烃受体（AHR）配体和丁酸盐，促进通过胰ILC的IL-22分泌，其诱导内分泌细胞表达MBD14。疑难生微生物群和低亲和力AHR等位基因解释了NOD小鼠中观察到的MBD14的缺陷胰腺表达。我们的研究揭示了胰腺和内分泌细胞之间尚未认定的串扰，对预防自身免疫性糖尿病发育至关重要。

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