Type 1 diabetes is the outcome of an autoimmune T cell response that destroys the insulin-producing b cells within the pancreas. The early stage of the disease--known as insulitis--is marked by infiltration of pancreatic islets by T cells, and, in an ironic twist, Frigerio et al. suggest that b cells may themselves be partly responsible. Exposure of a b cell line to a mix of inflammatory cytokines (IFN-g, IL1-b and TNF-a) stimulated the production of chemokines, proteins that orchestrate the migration of leukocytes. The same assortment of chemokines was detected in islets from mice with an induced form of insulitis; in culture, these chemokines stimulated migration of T cells isolated from prediabetic mice. This chemotaxis depended most strongly on the CXCR3 receptor and corresponded with delayed induction of diabetes in CXCR3-deficient mice. -- SJS
Nature Med. 8, 1414 (2002).
