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Arq Bras Endocrinol Metabol. 2008 Mar;52(2):156-65.

Mediators and mechanisms of pancreatic beta-cell death in type 1 diabetes.

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  • 1Laboratory of Experimental Medicine, Universit√© Libre de Bruxelles, Brussels, Belgium.

Abstract

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.

PMID:
18438526
[PubMed - indexed for MEDLINE]
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