Grant: Operating Grant - Priority Announcement: Infection and Immunity (Bridge Funding)

In the past decade, childhood type 1 diabetes, now mostly referred as type 1 diabetes (DT1), has increased dramatically world-wide. However the mechanisms underlying diabetes onset are poorly documented. Nonobese diabetic (NOD) mice spontaneously develop DT1, and therefore represent an excellent model that mirrors many features of the pathogenesis of the disease in DT1. Importantly, specialized cells called dendritic cells (DCs) act to dampen unwanted immune responses and promote regulatory T cells (Treg) function in order to prevent diseases onset. Abnormal function of DCs has been reported to play a critical role in initiation and progression of DT1. Many proteins influence the normal set-point of DCs. Recent research indicates that augmenting the function of a protein called Stat5b leads to increased numbers of beneficial Treg in mice. Our proposal seeks to determine if constitutively active Stat5b expressed in DCs can suppress the development of juvenile diabetes in a well-characterized NOD mouse model. If successful, this approach would spur the development of new therapies for patients with childhood type 1 diabetes.