By integrating previous findings regarding the Th17-producing cytokines IL-22, IL-17A/F, and GM-CSF, which have been shown to either ameliorate or exacerbate colitis phenotypes (Tables 1–3), we summarize their dual effects: a protective role via direct effects on IECs and a pathogenic role mediated indirectly through myeloid cells (Fig. 4). Here, IL17A is linked to colitis.