In our study, the phenotype and the function of plasmablasts were characterized as the following: (1) abundant expression of antigen-presenting proteins (HLA-II and CD86) with a negative association between CD86 expression and beta cell function; (2) association of increased plasmablasts and beta cell damage during the progression of T1D in both patients and mice; (3) synergistic effect of plasmablasts and T cells in accelerating T1D onset and in promoting beta cell apoptosis. This evidence concerns the gene CD86 and type 1 diabetes mellitus.