Autoimmune Diabetes in the NOD Mouse: An Essential Role of Fas‐FasL Signaling in β Cell Apoptosis | Zendy

SILVA DIEGO G. | Zendy; SOCHA LUIS | Zendy; CHARLTON BRETT | Zendy; COWDEN WILLIAM | Zendy; PETROVSKY NIKOLAI | Zendy

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Autoimmune Diabetes in the NOD Mouse: An Essential Role of Fas‐FasL Signaling in β Cell Apoptosis

Author(s) -

SILVA DIEGO G.,

SOCHA LUIS,

CHARLTON BRETT,

COWDEN WILLIAM,

PETROVSKY NIKOLAI

Publication year - 2003

Publication title -

annals of the new york academy of sciences

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.712

H-Index - 248

eISSN - 1749-6632

pISSN - 0077-8923

DOI - 10.1196/annals.1288.018

Subject(s) - fas ligand , apoptosis , beta cell , programmed cell death , immunology , nod mice , pancreatic islets , microbiology and biotechnology , beta (programming language) , signal transduction , cancer research , autoimmunity , biology , medicine , islet , diabetes mellitus , immune system , endocrinology , genetics , computer science , programming language

A bstract : 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.

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