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 |
|---|---|
| Pages (from-to) | 373-382 |
| Number of pages | 10 |
| Journal | Nature Immunology |
| Volume | 3 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 2002 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology
Cite this
Target cell defense prevents the development of diabetes after viral infection. / Flodström, Malin; Maday, Amy; Balakrishna, Deepika; Cleary, Mary Malo; Yoshimura, Akihiko; Sarvetnick, Nora.
In: Nature Immunology, Vol. 3, No. 4, 2002, p. 373-382.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Target cell defense prevents the development of diabetes after viral infection
AU - Flodström, Malin
AU - Maday, Amy
AU - Balakrishna, Deepika
AU - Cleary, Mary Malo
AU - Yoshimura, Akihiko
AU - Sarvetnick, Nora
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0036222240&partnerID=8YFLogxK
U2 - 10.1038/ni771
DO - 10.1038/ni771
M3 - Article
C2 - 11919579
AN - SCOPUS:0036222240
VL - 3
SP - 373
EP - 382
JO - Nature Immunology
JF - Nature Immunology
SN - 1529-2908
IS - 4
ER -