As predicted from the studies employing genetic ablation of CD1d expression, or the aGalCer iNKT agonist, NKT14 mediated depletion of iNKT cells led to significantly accelerated onset of T1D in NOD mice (P>0.01 Log-Rank (Mantel-Cox)), while their activation mediated by repeated administration of the NKT14m antibody partially protected and significantly delayed disease onset (P<0.05 Log Rank Mantel-Cox) (Fig 3). The gene discussed is CD1D; the disease is type 1 diabetes mellitus.