Coxsackievirus B Tailors the Unfolded Protein Response to Favour Viral Amplification in Pancreatic β Cells

Journal of Innate Immunity
Maikel L ColliAnne Op de Beeck

Abstract

Type 1 diabetes (T1D) is an autoimmune disease characterized by islet inflammation and progressive pancreatic β cell destruction. The disease is triggered by a combination of genetic and environmental factors, but the mechanisms leading to the triggering of early innate and late adaptive immunity and consequent progressive pancreatic β cell death remain unclear. The insulin-producing β cells are active secretory cells and are thus particularly sensitive to endoplasmic reticulum (ER) stress. ER stress plays an important role in the pathologic pathway leading to autoimmunity, islet inflammation, and β cell death. We show here that group B coxsackievirus (CVB) infection, a putative causative factor for T1D, induces a partial ER stress in rat and human β cells. The activation of the PERK/ATF4/CHOP branch is blunted while the IRE1α branch leads to increased spliced XBP1 expression and c-Jun N-terminal kinase (JNK) activation. Interestingly, JNK1 activation is essential for CVB amplification in both human and rat β cells. Furthermore, a chemically induced ER stress preceding viral infection increases viral replication, in a process dependent on IRE1α activation. Our findings show that CVB tailors the unfolded protein response in β ce...Continue Reading

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Citations

Apr 2, 2020·Infection and Immunity·Sharon K Kuss-Duerkop, A Marijke Keestra-Gounder
Jun 2, 2020·Diabetes, Obesity & Metabolism·Alexandra Coomans de BrachèneDecio L Eizirik
Feb 14, 2021·International Journal of Molecular Sciences·Cristina Cosentino, Romano Regazzi
Feb 7, 2021·Biology·Moses New-AaronNatalia A Osna
Mar 9, 2021·Frontiers in Endocrinology·Jon D PiganelliEddie A James
May 6, 2021·Diabetes·Teresa Rodriguez-CalvoEmily K Sims

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