Immunology

Fatal Attraction

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Science  13 Dec 2002:
Vol. 298, Issue 5601, pp. 2095
DOI: 10.1126/science.298.5601.2095a

Type 1 diabetes is the outcome of an autoimmune T cell response that destroys the insulin-producing β 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 β cells may themselves be partly responsible. Exposure of a β cell line to a mix of inflammatory cytokines (IFN-γ, IL1-β and TNF-α) 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

NatureMed. 8, 1414 (2002).

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