Abstract
AbstractType 1 diabetes results from the poorly understood process of islet autoimmunity, which ultimately leads to the loss of functional pancreatic beta cells. Mounting evidence supports the notion that the activation and evolution of islet autoimmunity in genetically susceptible people is contingent upon early life exposures affecting the islets, especially beta cells. Here, we review some of the recent advances and studies that highlight the roles of these changes as well as antigen presentation and stress response pathways in beta cells in the onset and propagation of the autoimmune process in type 1 diabetes. Future progress in this area holds promise for advancing islet- and beta cell-directed therapies that could be implemented in the early stages of the disease and could be combined with immunotherapies.
Graphical Abstract
Funder
FEDER
Research Manitoba
Health Sciences Centre Foundation Winnipeg
NIH-NIDDK
Canadian Institutes of Health Research
End Diabetes 2022 Award from Diabetes Canada
Genome Canada
Wellcome Trust Investigator Award
Innovation Canada John R. Evans Leader Award
Red Española de Supercomputación
CRCHUM start-up funds
UK MRC Programme grant
Juvenile Diabetes Research Foundation United States of America
Diabetes UK Project grant
ISCIII and FEDER
Praespero
MINECO
Generalitat de Catalunya
Alberta Diabetes Foundation
Publisher
Springer Science and Business Media LLC
Subject
Endocrinology, Diabetes and Metabolism,Internal Medicine
Cited by
6 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献