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Nat Immunol. 2002 Apr;3(4):373-82. Epub 2002 Mar 4.

Target cell defense prevents the development of diabetes after viral infection.

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1
Department of Immunology, IMM-23, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA.

Abstract

The mechanisms that regulate susceptibility to virus-induced autoimmunity remain undefined. We establish here a fundamental link between the responsiveness of target pancreatic beta cells to interferons (IFNs) and prevention of coxsackievirus B4 (CVB4)-induced diabetes. We found that an intact beta cell response to IFNs was critical in preventing disease in infected hosts. The antiviral defense, raised by beta cells in response to IFNs, resulted in a reduced permissiveness to infection and subsequent natural killer (NK) cell-dependent death. These results show that beta cell defenses are critical for beta cell survival during CVB4 infection and suggest an important role for IFNs in preserving NK cell tolerance to beta cells during viral infection. Thus, alterations in target cell defenses can critically influence susceptibility to disease.

PMID:
11919579
DOI:
10.1038/ni771
[Indexed for MEDLINE]
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