GSE106083
Aryl Hydrocarbon Receptor Preferentially Marks and Promotes Gut Regulatory T Cells
Here, we generated mouse genetic models to ablate or activate Ahr expression specifically in Tregs. We showed that Ahr was expressed more abundantly by peripherally induced Treg (pTregs) in the gut than by Tregs in other lymphoid organs, and its expression was independent of microbiota. Ahr was important for Treg gut homing and function. Ahr inhibited pro-inflammatory cytokines produced by Tregs but was dispensable for Treg stability. Furthermore, Ahr-expressing Tregs had enhanced in vivo suppressive activity compared to Tregs lacking Ahr expression in a T cell transfer model of colitis. Our data suggest that Ahr signaling in Tregs may be important for gut immune homeostasis. Overall design: RNA-seq (2 replicates) and ATAC-seq (2 replicates) analysis of large intestine regulatory T cells from Ahr wildtype and knockout mice.