Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by T and B cell activation and circulating autoantibodies. Common early causes of mortality include kidney disease and infection, while there is a striking increase in atherosclerosis risk for those surviving more than a year after diagnosis. Despite identification of this increased risk more than 40 years ago, mechanisms for SLE-accelerated atherosclerosis remain elusive. The B6.Sle1.2.3 (B6.SLE) mouse model of SLE contains three genetic loci that confer SLE susceptibility. Transplantation of bone marrow from B6.Sle1.2.3 into LDLr-/- mice results in increased atherosclerosis accompanied by more CD4+ T cells in the lesions, pointing to T cell dysregulation as a contributing factor. We confirmed a central role for CD4+ T cells in this process by demonstrating that transfer of B6.SLE CD4+ T cells into Rag-/-, LDLr-/- mice resulted in increased atherosclerosis compared to B6 CD4+ T cells. In the current study, we hypothesized that acceleration of atherosclerosis in SLE is due to resistance of B6.SLE CD4+ effector T cells (Teff) to suppression by regulatory T cells (Treg). Our data show that, although B6.SLE Treg have normal suppressive capacity, B6.SLE Teff are resistant to this suppression. In co-transfer experiments, results suggested an IL-17-mediated mechanism, by which B6.SLE Teff elicit increased IL-17 production by B6 Treg, much like levels produced by B6.SLE Treg.