CXCR3 and colitis: Also, T‐bet directly activates Th1‐specific chemokine receptors, such as CXCR3 and CCR5, which are critical for homing to inflamed tissues.[2] In the innate immune system, T‐bet deficiency controls the response of the mucosal immune system to commensal bacteria and increases susceptibility to colitis.[14] Furthermore, T‐bet is a central transcriptional regulator for intraepithelial lymphocyte (IEL) development and controls susceptibility to chemically induced colitis.[15] Besides in these immune cells, the function of T‐bet in intestinal epithelial cells has not been reported.