Abstract
Despite evidence that both Fas and FasL can be expressed in pancreatic islets, there has been considerable controversy regarding the potential role of Fas signaling in autoimmune β cell death. Using the HIPFasL model, we have been able to demonstrate that, in the presence of an inflammatory infiltrate, FasL-expressing β cells are exquisitely sensitive to Fas-mediated apoptosis and that this can be blocked by preventing FasL-Fas interaction. This points to a highly important role of Fas-FasL interaction in autoimmune β cell death.
Original language | English |
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Pages (from-to) | 161-165 |
Number of pages | 5 |
Journal | Annals of the New York Academy of Sciences |
Volume | 1005 |
DOIs | |
Publication status | Published - 2003 |