Image-guided analyses reveal that non-CD4 splenocytes contribute to CD4+ T cell-mediated inflammation leading to islet destruction by altering their local function and not systemic trafficking patterns.

Recruitment of CD4(+) T cells into islets is a critical component of islet inflammation (insulitis) leading to type 1 diabetes; therefore, determining if conditions used to treat diabetes change their trafficking patterns is relevant to the outcome. Cotransfer of CD4(+)BDC2.5 (BDC) cells with non-CD4 splenocytes obtained from newly diabetic NOD mice, but not when they are transferred alone, induces accelerated diabetes.