Abstract
The mechanisms that regulate susceptibility to virus-induced autoimmunity remain undefined. We establish here a fundamental link between the responsiveness of target pancreatic β cells to interferons (IFNs) and prevention of coxsackievirus B4 (CVB4)-induced diabetes. We found that an intact β cell response to IFNs was critical in preventing disease in infected hosts. The antiviral defense, raised by β cells in response to IFNs, resulted in a reduced permissiveness to infection and subsequent natural killer (NK) cell-dependent death. These results show that β cell defenses are critical for β cell survival during CVB4 infection and suggest an important role for IFNs in preserving NK cell tolerance to β cells during viral infection. Thus, alterations in target cell defenses can critically influence susceptibility to disease.
Original language | English |
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Pages (from-to) | 373-382 |
Number of pages | 10 |
Journal | Nature Immunology |
Volume | 3 |
Issue number | 4 |
DOIs | |
Publication status | Published - 2002 Apr |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology