CD4 and type 1 diabetes mellitus: These observations exposed a potential mechanism for the MHC class II-associated susceptibility and resistance to T1D, whereby anti-diabetogenic MHC class II alleles (e.g., I-Ab in mice and DQ6 in humans) would exploit the MHCII promiscuity of disease-initiating, 4.1-like CD4+ T-cell specificities to abort the pathogenic activity of their pro-diabetogenic counterparts (e.g., I-Ag7 in mice and DQ2/DQ8 in humans).