Fas ligand drives insulitis in the non-obese diabetic mouse model of type 1 diabetes (T1D) and negatively regulates IL-10-producing (IL-10^pos) CD5⁺ B cells in pancreata. Relevance of these phenomena to the human disease is poorly understood. Here, using splenocytes from T1D, autoantibody (Ab⁺), and non-diabetic (ND) human subjects, we show that a subpopulation of CD5⁺ B cells that is characterized by expression of FasL (FasL^hiCD5⁺) was significantly elevated in T1D subjects, many of whom had significantly reduced frequency of IL-10^posCD5⁺ B cells compared to Ab⁺ subjects. The majority of FasL^hiCD5⁺ B cells did not produce cytokines and were more highly resistant to activation-induced cell death than their IL-10^posCD5⁺ counterparts. These results associate expansion of FasL-expressing CD5⁺ B cells with T1D and lay the groundwork for future mechanistic studies to understand specific role in disease pathogenesis.