Apoptosis of Human Islet Cells by Cytokines
Immune Network
;
: 113-117, 2012.
Article
Dans Anglais
| WPRIM
| ID: wpr-216355
ABSTRACT
FasL, perforin, TNFalpha, IL-1 and NO have been considered as effector molecule(s) leading to beta-cell death in autoimmune diabetes. However, the real culprit(s) of beta-cell destruction have long been elusive despite intense investigation. Previously we have suggested IFNgamma/TNFalpha synergism as the final effector molecules in autoimmune diabetes of NOD mice. A combination of IFNgamma and TNFalpha but neither cytokine alone, induced classical caspase-dependent apoptosis in murine insulinoma and pancreatic islet cells. IFNgamma treatment conferred susceptibility to TNFalpha-induced apoptosis on otherwise resistant murine insulinoma cells by STAT1 activation followed by IRF-1 induction. Here we report that IFNgamma/TNFalpha synergism induces apoptosis of human pancreatic islet cells. We also observed STAT1 activation followed by IRF-1 induction by IFNgamma treatment in human islet cells. Taken together, we suggest that IFNgamma/TNFalpha synergism could be involved in human islet cell death in type 1 diabetes, similar to murine type 1 diabetes.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Auto-immunité
/
Cytokines
/
Ilots pancréatiques
/
Interleukine-1
/
Facteur de nécrose tumorale alpha
/
Souris de lignée NOD
/
Apoptose
/
Diabète de type 1
/
Perforine
/
Insulinome
Limites du sujet:
Animaux
/
Humains
langue:
Anglais
Texte intégral:
Immune Network
Année:
2012
Type:
Article
Documents relatifs à ce sujet
MEDLINE
...
LILACS
LIS