par Pirot, Pierre 
;Cardozo, Alessandra K ;Eizirik, Decio L.
Référence Arquivos brasileiros de endocrinologia e metabologia, 52, 2, page (156-165)
Publication Publié, 2008
;Cardozo, Alessandra K ;Eizirik, Decio L. Référence Arquivos brasileiros de endocrinologia e metabologia, 52, 2, page (156-165)
Publication Publié, 2008
Article révisé par les pairs
| Résumé : | Type 1 diabetes mellitus (T1D) is characterized by severe insulin deficiency resulting from chronic and progressive destruction of pancreatic beta-cells by the immune system. The triggering of autoimmunity against the beta-cells is probably caused by environmental agent(s) acting in the context of a predisposing genetic background. Once activated, the immune cells invade the islets and mediate their deleterious effects on beta-cells via mechanisms such as Fas/FasL, perforin/granzyme, reactive oxygen and nitrogen species and pro-inflammatory cytokines. Binding of cytokines to their receptors on the beta-cells activates MAP-kinases and the transcription factors STAT-1 and NFkappa-B, provoking functional impairment, endoplasmic reticulum stress and ultimately apoptosis. This review discusses the potential mediators and mechanisms leading to beta-cell destruction in T1D. |
