CD4 and inflammatory bowel disease: Together, our data support a beneficial role, and possibly a requirement, for Th17 cells and cells expressing the gut homing marker integrin β7 in protective immunity to C. difficile that may help explain the failure of drugs targeting IL17A to provide benefit in IBD.18 Further research should explore contributions of C. difficile overgrowth and low-level toxin production to dysbiosis, gastrointestinal symptoms and perturbations in the memory CD4+ T cell repertoire in IBD patients.