To confirm the hypothesis that IFN-I contributes to ileal inflammation in Atg16l1ΔIEC mice independent of an exogenous IL-22 stimulus, we performed a 2% DSS colitis with either anti-IFNAR or with corresponding IgG control at days 0, 2, 4, and 6 (Fig. S5 C) in the without IL-22 injection. This evidence concerns the gene IL22 and colitis.