查看文章

A polymorphism in the autophagy gene Atg16l1 is associated with susceptibility to inflammatory bowel disease (IBD); however, it remains unclear how autophagy contributes to intestinal immune homeostasis. Here, we demonstrate that autophagy is essential for maintenance of balanced CD4⁺ T cell responses in the intestine. Selective deletion of Atg16l1 in T cells in mice resulted in spontaneous intestinal inflammation that was characterized by aberrant type 2 responses to dietary and microbiota antigens, and by a loss of Foxp3⁺ T_reg cells. Specific ablation of Atg16l1 in Foxp3⁺ T_reg cells in mice demonstrated that autophagy directly promotes their survival and metabolic adaptation in the intestine. Moreover, we also identify an unexpected role for autophagy in directly limiting mucosal T_H2 cell expansion. These findings provide new insights into the reciprocal control of distinct intestinal T_H cell responses by autophagy, with important implications for understanding and treatment of chronic inflammatory disorders.

DOI: http://dx.doi.org/10.7554/eLife.12444.001