Hobit- and Blimp-1-driven CD4 tissue-resident memory T cells control chronic intestinal inflammation.

Although tissue-resident memory T cells (T cells) have been shown to regulate host protection in infectious disorders, their function in inflammatory bowel disease (IBD) remains to be investigated. Here we characterized T cells in human IBD and in experimental models of intestinal inflammation. Pro-inflammatory T cells accumulated in the mucosa of patients with IBD, and the presence of CD4CD69CD103 T cells was predictive of the development of flares. In vivo, functional impairment of T cells in mice with double knockout of the T-cell-associated transcription factors Hobit and Blimp-1 attenuated disease in several models of colitis, due to impaired cross-talk between the adaptive and innate immune system. Finally, depletion of T cells led to a suppression of colitis activity. Together, our data demonstrate a central role for T cells in the pathogenesis of chronic intestinal inflammation and suggest that these cells could be targets for future therapeutic approaches in IBD.