Our result shows that the transfer of Yeti iNKT cells prevents pathogenic MLN Foxp3−CD25+CD4+ T cell differentiation in Jα18 KO recipient mice (they lack iNKT cells but express glycolipid Ag-presenting CD1d), suggesting that Yeti iNKT cells might be activated by glycolipid Ags derived from intestinal commensal bacteria during DSS-induced intestinal inflammation. Here, CFDP1 is linked to gastroenteritis.