Here, we show that AIEC, but not SFB, is associated with Th17 responses that exacerbate disease and promote ileocolitis in an AGR2-deficient background, highlighting the requirement for ER stress and potentially other factors in shaping pathogenic Th17 cell activation in this model.48 While increased Th17 cells parallels previous observations establishing the connection between AIEC and pathogenic Th17 cell induction in various genetic backgrounds,5,8,49 our depletion studies reveal an alternate model in which CD103+ DCs regulate IL-23-dependent disease associated with ER stress. Here, IL23A is linked to ileocolitis.