NOD.CD11cStat5b-CA mice were protected from diabetes. Stat5b-CA.DCs induced antigen specific Treg differentiation, enhanced Treg suppressive activity and promoted Th2/Tc2 immune deviation. Stat5b-CA.DC educated CD4+CD25− T cells delay diabetes onset whereas Stat5b-CA.DC educated Tregs blocked ongoing diabetes. A single injection of Stat5b-CA.DCs halted diabetes progression and educated their splenocytes to loose their diabetogenic potential.