Type 1 diabetes results, at least in part, from invasion of pancreatic islets by T lymphocytes and antigen presenting cells (APCs) including macrophages and dendritic cells (DCs). What drives the migration of these immune cells into the islets remains unknown. A key step in the arrival of immune cells to a specific location is adhesion to the inner lining of blood vessels and then transit through the vessel wall into the surrounding tissue. Chemokines are important proteins in this process. Chemokines that are expressed by the cells making up blood vessels alert immune cells to nearby inflammation and assist the immune cells with leaving the vessel. One chemokine with this function is CCL21. Activated APCs and naïve T cells express the surface receptor CCR7 that binds CCL21 and directs the cells towards environments where CCL21 is present. We found through profiling of genes expressed in the islets of T1D subjects in the nPOD cohort that CCL21 levels are elevated in the islets that have been infiltrated by T cells but not islets lacking T cells. We hypothesize that endothelial cells of the islet are expressing CCL21 and that drugs that block CCL21 activity can prevent destructive immune invasion of the islets. This study is designed to determine where in the islet environment CCL21 protein is found. Since immune infiltrates are focal, we anticipate that CCL21 will co-localize with regions of the islet where APCs or naïve T cells have infiltrated.