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美国哈佛医学院Diane Mathis团队发现肠道菌群通过RORγ+调节性T（Treg）细胞信使促进远端组织再生。这一成果发表在2023年2月22日出版的《免疫》杂志上。

他们发现高度相似的微生物群依赖性Treg细胞群促进了肠外部位的组织再生，特别是急性损伤的骨骼肌和脂肪肝。由组织损伤引发炎症介导因子结合MHC II类依赖性T细胞活化，以驱动肠道来源的RORγ+ Treg细胞在损伤肌肉中的积累，其中它们调节早期炎症的动力学和期限，并帮助平衡局部干细胞的增殖与分化。控制T细胞中IL-17A的产生是受损组织中RORγ+ Treg细胞变阻功能的主要机制。

他们的研究结果强调了肠道训练的Treg细胞使者在控制对非粘膜组织无菌损伤反应方面的重要性。

据介绍，特定的微生物信号诱导对肠道稳态至关重要的独特RORγ+ Treg细胞池的分化。

附：英文原文

Title: The gut microbiota promotes distal tissue regeneration via RORγ+ regulatory T cell emissaries

Author: Bola S. Hanna, Gang Wang, Silvia Galván-Pea, Alexander O. Mann, Ricardo N. Ramirez, Andrés R. Muoz-Rojas, Kathleen Smith, Min Wan, Christophe Benoist, Diane Mathis

Issue&Volume: 2023-02-22

Abstract: Specific microbial signals induce the differentiation of a distinct pool of RORγ+ regulatory T (Treg) cells crucial for intestinal homeostasis. We discovered highlyanalogous populations of microbiota-dependent Treg cells that promoted tissue regenerationat extra-gut sites, notably acutely injured skeletal muscle and fatty liver. Inflammatorymeditators elicited by tissue damage combined with MHC-class-II-dependent T cell activationto drive the accumulation of gut-derived RORγ+ Treg cells in injured muscle, wherein they regulated the dynamics and tenor of earlyinflammation and helped balance the proliferation vs. differentiation of local stemcells. Reining in IL-17A-producing T cells was a major mechanism underlying the rheostaticfunctions of RORγ+ Treg cells in compromised tissues. Our findings highlight the importance of gut-trainedTreg cell emissaries in controlling the response to sterile injury of non-mucosaltissues.

DOI: 10.1016/j.immuni.2023.01.033

Source: https://www.cell.com/immunity/fulltext/S1074-7613(23)00045-6

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