title: Autoimmune diabetes in the NOD mouse: an essential role of Fas-FasL signaling in beta cell apoptosis.
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 beta cell death. Using the HIPFasL model, we have been able to demonstrate that, in the presence of an inflammatory infiltrate, FasL-expressing beta 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 beta cell death.
authors.affiliation: Autoimmunity Research Unit, The Canberra Hospital, Canberra, Australia.
authors.forename: Diego G
authors.initials: DG
authors.lastname: Silva
authors.forename: Luis
authors.initials: L
authors.lastname: Socha
authors.forename: Brett
authors.initials: B
authors.lastname: Charlton
authors.forename: William
authors.initials: W
authors.lastname: Cowden
authors.forename: Nikolai
authors.initials: N
authors.lastname: Petrovsky
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D016207:Cytokines / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins / Q000502:physiology*; D051379:Mice; D016688:Mice, Inbred NOD; D008822:Mice, Transgenic; D015398:Signal Transduction; D019014:fas Receptor / Q000502:physiology*
chemical_list: D016207:Cytokines; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D019014:fas Receptor