Regulation of gut mucosal homeostasis by autophagy in dendritic cells

本研究表明，在稳态条件下，肠道相关淋巴组织（GALT）中的树突状细胞（dc）可组成性地诱导自噬，其诱导依赖于共生菌的吞噬。在结肠炎模型中，dc特异性自噬缺陷小鼠在恢复阶段表现出粘膜完整性的延迟恢复。自噬缺陷的GALT dc在结肠炎恢复期显示细胞内共生细菌增加，IL-6和TNF-〓的产生增加，IL-23的产生减少。重要的是，在自噬缺陷小鼠中，由IL-23诱导的组织重塑细胞因子IL-22的产生大大减少。综上所述，这些结果表明GALT dc的组成性自噬是由共生菌的细胞内识别诱导的，并提示自噬在结肠炎的粘膜愈合中起重要作用。

We here showed that autophagy is constitutively induced in dendritic cells (DCs) in the gut-associated lymphoid tissues (GALT) under steady-state conditions and the induction is dependent on the engulfment of commensal bacteria. In a colitis model, DC-specific autophagy-deficient mice showed a delayed restoration of mucosal integrity in a recovery phase. Autophagy-deficient GALT DCs revealed increased intracellular commensal bacteria, increased production of IL-6 and TNF-〓, and reduced production of IL-23 in the recovery phase of colitis. Importantly, the production of tissue-remodeling cytokine IL-22, which is induced by IL-23, was much reduced in the autophagy-deficient mice. Collectively, these results indicate that constitutive autophagy in GALT DCs is induced by the intracellular recognition of commensal bacteria, and suggest that the autophagy plays an important role in mucosal healing of colitis.