Blocking IAg


Journal

Life sciences
ISSN: 1879-0631
Titre abrégé: Life Sci
Pays: Netherlands
ID NLM: 0375521

Informations de publication

Date de publication:
01 Jan 2022
Historique:
received: 09 09 2021
revised: 16 11 2021
accepted: 22 11 2021
pubmed: 30 11 2021
medline: 11 1 2022
entrez: 29 11 2021
Statut: ppublish

Résumé

Sjögren's syndrome (SjS) is an autoimmune disease with a strong genetic association. To date, no vaccine or therapeutic agent exists to cure SjS, and patients must rely on lifelong therapies to treat symptoms. Human leukocyte antigens (HLA) are primary susceptibility loci that form the genetic basis for many autoimmune diseases, including SjS. In this study, we sought to determine whether blocking MHC class II IAg Mapping of the antigenic epitopes of Ro60 autoantigen to IAg Specific peptides of Ro60 autoantigen were identified to bind to IAg This study presents a novel therapeutic approach for SjS by identifying small molecules capable of inhibiting T cell response via antigen-specific presentation. CQN is supported financially in part by PHS grants AI130561, DE026450, and DE028544 from the National Institutes of Health.

Sections du résumé

BACKGROUND BACKGROUND
Sjögren's syndrome (SjS) is an autoimmune disease with a strong genetic association. To date, no vaccine or therapeutic agent exists to cure SjS, and patients must rely on lifelong therapies to treat symptoms. Human leukocyte antigens (HLA) are primary susceptibility loci that form the genetic basis for many autoimmune diseases, including SjS. In this study, we sought to determine whether blocking MHC class II IAg
METHODS METHODS
Mapping of the antigenic epitopes of Ro60 autoantigen to IAg
FINDINGS RESULTS
Specific peptides of Ro60 autoantigen were identified to bind to IAg
INTERPRETATION CONCLUSIONS
This study presents a novel therapeutic approach for SjS by identifying small molecules capable of inhibiting T cell response via antigen-specific presentation.
FUNDING BACKGROUND
CQN is supported financially in part by PHS grants AI130561, DE026450, and DE028544 from the National Institutes of Health.

Identifiants

pubmed: 34843735
pii: S0024-3205(21)01169-3
doi: 10.1016/j.lfs.2021.120182
pmc: PMC8883604
mid: NIHMS1780885
pii:
doi:

Substances chimiques

Alkanes 0
Antimetabolites, Antineoplastic 0
Histocompatibility Antigens Class II 0
I-A g7 antigen 0
Polycyclic Compounds 0
Azaguanine Q150359I72

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

120182

Subventions

Organisme : NIDCR NIH HHS
ID : R01 DE026450
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE028544
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI130561
Pays : United States

Informations de copyright

Copyright © 2021. Published by Elsevier Inc.

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Auteurs

Shivai Gupta (S)

Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA.

Danmeng Li (D)

Department of Pathology, Immunology & Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL, USA.

David A Ostrov (DA)

Department of Pathology, Immunology & Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL, USA.

Cuong Q Nguyen (CQ)

Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA; Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL, USA; Center of Orphaned Autoimmune Diseases, University of Florida, Gainesville, FL, USA. Electronic address: nguyenc@ufl.edu.

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Classifications MeSH