In summary, we demonstrated ATF3 as a regulator of T<sub>FH</sub> cells in the gut, which may represent a potential immunotherapeutic target in colitis.
Loss of ATF3 led to decreased crypt numbers, more shortened colon length, impaired ileal fucosylation at the steady state, and lethal disease activity during DSS-induced colitis which can be effectively ameliorated by rectal transplantation of wild-type colonic organoids.