There is a need for novel treatments for patients with inflammatory bowel disease (IBD) who do not respond to medical therapy. It is likely that IBD arises from dysfunctional interactions between the mucosal immune system and the gut microbiome, and manipulation of this interaction is therefore a promising therapeutic target. Signaling through the T cell receptor (TCR) may have a powerful role in controlling inflammation in IBD, as chimeric antigen receptor regulatory T cells (Tregs) which recognize colitis-associated antigens have been demonstrated to control inflammation in mouse models.