CD4 and type 1 diabetes mellitus: These striking observations raise several open questions: (a) what structural features distinguish DQ molecules associated with risk for T1D; (b) why do heterozygotes have even greater risk for T1D than individuals homozygous for DQ2 or DQ8; (c) how do the autoreactive CD4+ T cells that mediate β cell destruction develop and escape negative selection in the thymus.