Abstract
Fas is an apoptosis-inducing surface receptor involved in controlling tissue homeostasis and function at multiple sites. Here we show that β cells from the pancreata of newly diagnosed insulin-dependent diabetes mellitus (IDDM) patients express Fas and show extensive apoptosis among those cells located in proximity to Fas ligand-expressing T lymphocytes infiltrating the IDDM islets. Normal human pancreatic β cells that do not constitutively express Fas, become strongly Fas positive after interleuken (IL)-β exposure, and are then susceptible to Fas-mediated apoptosis. N(G)-monomethyl-L- arginine, an inhibitor of nitric oxide (NO) synthase, prevents IL-β-induced Fas expression, whereas the NO donors sodium nitroprusside and nitric oxide releasing compound (NOC)-18, induce functional Fas expression in normal pancreatic β cells. These findings suggest that NO-mediated upregulation of Fas contributes to pancreatic β cell damage in IDDM.
Lingua originale | English |
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pagine (da-a) | 1193-1200 |
Numero di pagine | 8 |
Rivista | Journal of Experimental Medicine |
Volume | 186 |
DOI | |
Stato di pubblicazione | Pubblicato - 1997 |
Keywords
- Immunology
- Immunology and Allergy