Journal
CELL METABOLISM
Volume 19, Issue 5, Pages 883-890Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2014.03.001
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Funding
- Swedish Research Council [12234, 2010-2653, K2012-66X-14928-09-5]
- NovoNordisk
- Diabetes Wellness Foundation
- Ragnar Soderberg Foundation
- Swedish Diabetes Society
- Goran Gustafsson Foundation
- Family Ernfors Foundation
- OE&E Johanssons Foundation
- Osterlund Foundation
- Greta and Johan Kock Foundation
- King Gustav V's 80th Anniversary Foundation
- EU Integrated project BetaBat
- Knut and Alice Wallenberg Foundation
- EXODIAB
- Novo Nordisk Fonden [NNF14OC0010001] Funding Source: researchfish
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Type 2 diabetes is triggered by reduced insulin production, caused by genetic and environmental factors such as inflammation originating from the innate immune system. Complement proteins are a component of innate immunity and kill non-self cells by perforating the plasma membrane, a reaction prevented by CD59. Human pancreatic islets express CD59 at very high levels. CD59 is primarily known as a plasma membrane protein in membrane rafts, but most CD59 protein in pancreatic beta cells is intracellular. Removing extracellular CD59 disrupts membrane rafts and moderately stimulates insulin secretion, whereas silencing intracellular CD59 markedly suppresses regulated secretion by exocytosis, as demonstrated by TIRF imaging. CD59 interacts with the exocytotic proteins VAMP2 and Syntaxin-1. CD59 expression is reduced by glucose and in rodent diabetes models but upregulated in human diabetic islets, potentially reflecting compensatory reactions. This unconventional action of CD59 broadens the established view of innate immunity in type 2 diabetes.
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