Abstract CD137 is a T cell costimulatory molecule that increases cell survival and promotes cytokine production, and is a candidate gene (Tnfrsf9) in NOD.B10 Idd9.3 congenic mice. We have shown that Tregs constitutively expressing CD137 are the target of anti-CD137 antibody that protects NOD from diabetes. Here, we show that NOD.B10 Idd9.3 CD137pos, but not CD137neg or NOD, Tregs have increased in vivo survival. Mixed bone marrow chimera mice made with NOD and NOD.B10 Idd9.3 bone marrow showed that increased survival in Tregs expressing the B10, but not NOD, Tnfrsf9 allele was an intrinsic cellular effect. NOD.B10 Idd9.3 CD137pos Tregs also express more anti-apoptotic Bcl-xl than NOD Tregs. To understand the impact of increased survival of CD137pos Tregs on disease, we performed functional studies that showed that CD137pos Tregs are significantly more suppressive than CD137neg Tregs in-vitro. We show that CD137pos Tregs, not CD137neg Tregs or T effectors, are the primary producers of the alternatively spliced CD137 isoform, soluble CD137. Soluble CD137 directly suppressed effector T cells by binding to CD137L on T cells in an APC independent assay. The increased suppression of CD137pos Tregs was associated with increased production of soluble CD137 and these studies show the importance of CD137pos Tregs in T1D.