TY - JOUR TI - The autophagy gene Atg16l1 differentially regulates Treg and TH2 cells to control intestinal inflammation AU - Kabat, Agnieszka M AU - Harrison, Oliver J AU - Riffelmacher, Thomas AU - Moghaddam, Amin E AU - Pearson, Claire F AU - Laing, Adam AU - Abeler-Dörner, Lucie AU - Forman, Simon P AU - Grencis, Richard K AU - Sattentau, Quentin AU - Simon, Anna Katharina AU - Pott, Johanna AU - Maloy, Kevin J A2 - Dikic, Ivan VL - 5 PY - 2016 DA - 2016/02/24 SP - e12444 C1 - eLife 2016;5:e12444 DO - 10.7554/eLife.12444 UR - https://doi.org/10.7554/eLife.12444 AB - 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+ Treg cells. Specific ablation of Atg16l1 in Foxp3+ Treg 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 TH2 cell expansion. These findings provide new insights into the reciprocal control of distinct intestinal TH cell responses by autophagy, with important implications for understanding and treatment of chronic inflammatory disorders. KW - autophagy KW - IBD KW - mucosal immunology KW - T helper cells JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -