The role of Treg-mediated IL-6R signaling in epithelial cell biology
IL-6 has been shown to be crucial in promoting inflammation in the context of IBD. Our previous work demonstrated an impairment of the FOXP3-mediated interactions necessary for Tregs to suppress immune responses following incubation with IL-6. However, the precise role of IL-6 and its receptor (IL-6R) signaling in Tregs and the impact on other cell types during IBD pathogenesis remains to be studied. Here  we demonstrate that loss of the IL-6R on Tregs negatively impacts intestinal epithelial cell homeostasis, and suggests the alterations could be contributing to an exacerbated phenotype in an in vivo model of colitis. Overall design: RNA-seq profiling of cololnic IECs isolated from water or 2% DSS-treated conditional Treg IL-6RaKO mice and Treg WTcre mice (controls).