Notably, in the BDC2.5-transgenic NODRag model of autoimmune diabetes, anti-CD3 treatment has been shown to induce massive proliferation of an initially constrained population of BDC2.5+Foxp3+ Treg cells and long-term protection from diabetes development, which could be abrogated by subsequent DT-mediated Treg cell depletion (51). Here, FOXP3 is linked to diabetes mellitus.