FCGR2A and colitis: This is in agreement with similar observations in colon biopsies from ipilimumab-treated patients where Treg depletion was not apparent.25 29 32 37 and with studies in adult mice which show CTLA4 expression on Tregs is neither necessary for their suppressive function nor critical for preventing systemic inflammation.38 Both colitis models taken together suggest that the inflammatory mechanism of Fc-effector anti-CTLA4 in the context of FcγR engagement is driven more by effector T-cells than Tregs.