HLA-A02 restricted T-cell cross-reactivity to a microbial antigen

Molecular mimicry has been proposed to be a possible mechanism of induction of autoimmunity. In some cases, it is believed that such events could lead to a disease such as Type 1 diabetes (T1D). One of the primary MHC-I epitopes in the non-obese diabetic (NOD) mouse model of T1D has been identified...

Full description

Saved in:
Bibliographic Details
Main Authors: Alar Aints, Marina Šunina, Raivo Uibo
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Journal of Immunotoxicology
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/1547691X.2024.2373247
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1841525377934032896
author Alar Aints
Marina Šunina
Raivo Uibo
author_facet Alar Aints
Marina Šunina
Raivo Uibo
author_sort Alar Aints
collection DOAJ
description Molecular mimicry has been proposed to be a possible mechanism of induction of autoimmunity. In some cases, it is believed that such events could lead to a disease such as Type 1 diabetes (T1D). One of the primary MHC-I epitopes in the non-obese diabetic (NOD) mouse model of T1D has been identified as a peptide from the islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) protein. In humans, the most common MHC-I model allele is HLA-A02; based on this, the study here identified a potential HLA-A0201-restricted human IGRP epitope as YLKTNLFLFL and also found a homologous A0201-restricted peptide in an Enterococcal protein. Using cells obtained from healthy human donors, it was seen that after a 2-week incubation with the synthetic bacterial protein, healthy A0201+ donor CD8+ cells displayed increased staining for human IGRP-peptide-dextramer. On the other hand, in control cultures, no significant levels of dextramer-staining CD8+ T-cells were detectable. From these outcomes, it is possible to conclude that certain bacterial proteins may initiate CD8+ T-cell-mediated immune reaction toward homologous human antigens.
format Article
id doaj-art-6a3de060b104403b95e15c4a0de1500a
institution Kabale University
issn 1547-691X
1547-6901
language English
publishDate 2024-12-01
publisher Taylor & Francis Group
record_format Article
series Journal of Immunotoxicology
spelling doaj-art-6a3de060b104403b95e15c4a0de1500a2025-01-17T12:52:14ZengTaylor & Francis GroupJournal of Immunotoxicology1547-691X1547-69012024-12-0121110.1080/1547691X.2024.2373247HLA-A02 restricted T-cell cross-reactivity to a microbial antigenAlar Aints0Marina Šunina1Raivo Uibo2Department of Immunology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, EstoniaDepartment of Immunology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, EstoniaDepartment of Immunology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, EstoniaMolecular mimicry has been proposed to be a possible mechanism of induction of autoimmunity. In some cases, it is believed that such events could lead to a disease such as Type 1 diabetes (T1D). One of the primary MHC-I epitopes in the non-obese diabetic (NOD) mouse model of T1D has been identified as a peptide from the islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) protein. In humans, the most common MHC-I model allele is HLA-A02; based on this, the study here identified a potential HLA-A0201-restricted human IGRP epitope as YLKTNLFLFL and also found a homologous A0201-restricted peptide in an Enterococcal protein. Using cells obtained from healthy human donors, it was seen that after a 2-week incubation with the synthetic bacterial protein, healthy A0201+ donor CD8+ cells displayed increased staining for human IGRP-peptide-dextramer. On the other hand, in control cultures, no significant levels of dextramer-staining CD8+ T-cells were detectable. From these outcomes, it is possible to conclude that certain bacterial proteins may initiate CD8+ T-cell-mediated immune reaction toward homologous human antigens.https://www.tandfonline.com/doi/10.1080/1547691X.2024.2373247Autoimmunitycross-presentationType 1 diabetesmolecular mimicryimmunotoxin
spellingShingle Alar Aints
Marina Šunina
Raivo Uibo
HLA-A02 restricted T-cell cross-reactivity to a microbial antigen
Journal of Immunotoxicology
Autoimmunity
cross-presentation
Type 1 diabetes
molecular mimicry
immunotoxin
title HLA-A02 restricted T-cell cross-reactivity to a microbial antigen
title_full HLA-A02 restricted T-cell cross-reactivity to a microbial antigen
title_fullStr HLA-A02 restricted T-cell cross-reactivity to a microbial antigen
title_full_unstemmed HLA-A02 restricted T-cell cross-reactivity to a microbial antigen
title_short HLA-A02 restricted T-cell cross-reactivity to a microbial antigen
title_sort hla a02 restricted t cell cross reactivity to a microbial antigen
topic Autoimmunity
cross-presentation
Type 1 diabetes
molecular mimicry
immunotoxin
url https://www.tandfonline.com/doi/10.1080/1547691X.2024.2373247
work_keys_str_mv AT alaraints hlaa02restrictedtcellcrossreactivitytoamicrobialantigen
AT marinasunina hlaa02restrictedtcellcrossreactivitytoamicrobialantigen
AT raivouibo hlaa02restrictedtcellcrossreactivitytoamicrobialantigen