Circulating CD4 T cells specific for peptide epitopes of proinsulin and other autoantigens are markers of autoimmune beta cell destruction in type 1 diabetes, while the role of CD8 T cells is still largely unknown. Here we show that CD8 T cells of a diabetic patient--after rechallange with proinsulin peptides--secrete IFNgamma and granzyme B, markers of their effector capacity. On the other hand, CD8 T cells of the same patient in a "cross-talk" with proinsulin-specific CD4 T cells suppress their proliferation. If confirmed in larger numbers of subjects with beta-islet cell autoimmunity, these results may help us to understand the role of CD8 cells in disease progression and extend our knowledge of disease pathogenesis.