Islet autoimmunity in human type 1 diabetes: initiation and progression from the perspective of the beta cell

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Abstract
Type 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
Funding Information
  • FEDER
  • Research Manitoba (5351)
  • Health Sciences Centre Foundation Winnipeg
  • NIH-NIDDK (R01DK135268)
  • Canadian Institutes of Health Research (CIHR-IRSC TDP-186358, FDN-353029, FRN-168480, PJT-479038, PJT-479040, PJT-479641)
  • End Diabetes 2022 Award from Diabetes Canada (OG-3-22-5694-PT)
  • Genome Canada
  • Wellcome Trust Investigator award (212625/Z/18/Z)
  • Innovation Canada John R. Evans Leader Award (CFI 42649)
  • Red Española de Supercomputación
  • CRCHUM start-up funds
  • UK MRC Programme grant (MR/R022259/1)
  • Juvenile Diabetes Research Foundation United States of America (DT4-179512, JDRF 4-SRA-2023-1182-S-N)
  • Diabetes UK Project Grant (BDA16/0005485)
  • ISCIII and FEDER (PI15/0797, PIE14/00027)
  • Praespero
  • MINECO (PID2021-125493OB-I00)
  • Generalitat de Catalunya
  • Alberta Diabetes Foundation

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