Therefore, we hypothesized that while RORγt and BATF commonly regulate Th17 cell formation critically affecting, e.g., syngeneic colitis development (9, 11, 18, 31), in intestinal GvHD pathogenesis, however, RORγt is not involved in the formation of a second, previously as BATF-dependent described colitogenic T cell subset. This evidence concerns the gene BATF and graft versus host disease.