T cell movement into the islets in the pancreas, is a hallmark feature of Type 1 diabetes (T1D) that has been demonstrated on autopsy in human pancreas specimens and in mouse models of T1D such as the non-obese diabetic (NOD) mouse3-8. By determiningthe role that insulin receptor (IR)plays in this movement of the T cells may generate anew immunotherapeutic intervention for T1D, especially since chemotactic signaling and metabolic signaling are mediated by distinct parts of the IR9. Blocking IR mediated chemotaxis without affecting insulin binding and signaling would offer a new pharmacotherapeutic target, since it would effectively block T cell movement into the pancreas. Blocking T cell movement would stop or delay diabetes development in diabetes prone individuals and may allow for beta cell regeneration. Chemotaxis to the islets via IR expression is the hypothesis. To investigate this, we will examine T cells in human islets (control and T1D) for IR expression.