Silva Diego G, Socha Luis, Charlton Brett, Cowden William, Petrovsky Nikolai
Autoimmunity Research Unit, The Canberra Hospital, Canberra, Australia.
Ann N Y Acad Sci. 2003 Nov;1005:161-5. doi: 10.1196/annals.1288.018.
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.
尽管有证据表明Fas和FasL均可在胰岛中表达,但Fas信号在自身免疫性β细胞死亡中的潜在作用一直存在很大争议。利用HIPFasL模型,我们已经能够证明,在存在炎性浸润的情况下,表达FasL的β细胞对Fas介导的凋亡极为敏感,并且这可以通过阻止FasL-Fas相互作用来阻断。这表明Fas-FasL相互作用在自身免疫性β细胞死亡中起着非常重要的作用。