PDIA3 epitope-driven immune autoreactivity contributes to hepatic damage in type 2 diabetes.
Journal
Science immunology
ISSN: 2470-9468
Titre abrégé: Sci Immunol
Pays: United States
ID NLM: 101688624
Informations de publication
Date de publication:
12 08 2022
12 08 2022
Historique:
entrez:
19
8
2022
pubmed:
20
8
2022
medline:
24
8
2022
Statut:
ppublish
Résumé
A diet rich in saturated fat and carbohydrates causes low-grade chronic inflammation in several organs, including the liver, ultimately driving nonalcoholic steatohepatitis. In this setting, environment-driven lipotoxicity and glucotoxicity induce liver damage, which promotes dendritic cell activation and generates a major histocompatibility complex class II (MHC-II) immunopeptidome enriched with peptides derived from proteins involved in cellular metabolism, oxidative phosphorylation, and the stress responses. Here, we demonstrated that lipotoxicity and glucotoxicity, as driven by a high-fat and high-fructose (HFHF) diet, promoted MHC-II presentation of nested T and B cell epitopes from protein disulfide isomerase family A member 3 (PDIA3), which is involved in immunogenic cell death. Increased MHC-II presentation of PDIA3 peptides was associated with antigen-specific proliferation of hepatic CD4
Identifiants
pubmed: 35984892
doi: 10.1126/sciimmunol.abl3795
pmc: PMC9762167
mid: NIHMS1852669
doi:
Substances chimiques
Epitopes
0
Histocompatibility Antigens Class II
0
Peptides
0
Protein Disulfide-Isomerases
EC 5.3.4.1
PDIA3 protein, human
EC 5.3.4.1.
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
eabl3795Subventions
Organisme : NIAID NIH HHS
ID : R01 AI137198
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI146180
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
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