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...
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Taylor & Francis Group
2024-12-01
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Series: | Journal of Immunotoxicology |
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Online Access: | https://www.tandfonline.com/doi/10.1080/1547691X.2024.2373247 |
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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 |