Abstract:
:Immunologically privileged sites express Fas ligand (FasL), which protects them from attack by activated T cells that express Fas and die upon contact with FasL. In an attempt to protect nonobese diabetic mice (NOD) from autoimmune diabetes, we made FasL transgenic NOD mice using the beta cell-specific rat insulin-1 promoter. Surprisingly, these transgenic mice showed heightened sensitivity to diabetogenic T cells, which was due to self-destruction of beta cells upon T cell-mediated induction of Fas. Fas-negative NOD(lpr/lpr) animals were resistant to diabetogenic T cells and to spontaneous diabetes. Thus, induction of Fas expression on beta cells and their subsequent destruction constitutes the main pathogenic mechanism in autoimmune diabetes.
journal_name
Celljournal_title
Cellauthors
Chervonsky AV,Wang Y,Wong FS,Visintin I,Flavell RA,Janeway CA Jr,Matis LAdoi
10.1016/s0092-8674(00)80178-6subject
Has Abstractpub_date
1997-04-04 00:00:00pages
17-24issue
1eissn
0092-8674issn
1097-4172pii
S0092-8674(00)80178-6journal_volume
89pub_type
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