IL17A and colitis: This caused constitutive CD40-signaling in CD11c+ DCs and as a consequence, the DC-iTreg axis was altered and mice developed fatal colitis.24 This signal caused loss of intestinal CD103+ DCs, deficiency to generate iTregs and increased IL-17+IFNγ+ Th17/Th1 cells and pathogenic IFNγ+ Th1 cells.24,25