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Expression of a Novel Murine Type I IFN in the Pancreatic Islets Induces Diabetes in Mice¹

Galya Vassileva^*, Shu-Cheng Chen^*, Ming Zeng^*, Susan Abbondanzo^*, Kristian Jensen^*, Daniel Gorman, Bahige M. Baroudy, Ying Jiang, Nicholas Murgolo and Sergio A. Lira^2,*

Departments of ^* Immunology, Virology, and Bioinformatics, Schering-Plough Research Institute, Kenilworth, NJ 07033; and DNAX Research Institute, Palo Alto, CA 94304

IFN- belongs to a recently identified subclass of type I IFNs. In this study, we report the cloning and preliminary characterization of the murine homologue of IFN-. The gene encodes a 200-aa protein which is 38.5% homologous to human IFN-. Murine IFN- contains four cysteines in analogous positions to those observed in the IFN- and an additional fifth unique cysteine, C174. The murine gene is located on chromosome 4, where other type I murine IFN genes, IFN- and IFN-, are clustered. This region is syntenic with human chromosome 9 where the gene encoding IFN- and the type I IFN gene cluster are found. Mouse IFN- is expressed at low levels in peritoneal macrophages and its expression is up-regulated by dsRNA and IFN-. Similar to previously reported transgenic mice carrying type I and type II IFNs, transgenic mice overexpressing murine IFN- in the cells of the pancreas develop overt diabetes with hyperglycemia. Histological characterization of pancreatic islets from these transgenic mice showed inflammatory infiltrates with corresponding destruction of cells.

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