HLA-DR3 restricted environmental epitopes from the bacterium Clostridium tetani have T cell cross-reactivity to the SLE-related autoantigen SmD
HLA-DR3 (DR3) is one of the dominant HLA-DR alleles associated with systemic lupus erythematosus (SLE) susceptibility. Our previous studies showed multiple intramolecular DR3 restricted T cell epitopes in the Smith D (SmD) protein, from which we generated a non-homologous, bacterial epitope mimics l...
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| Published in | Frontiers in immunology Vol. 13; p. 928374 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Frontiers Media S.A
31.10.2022
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| Online Access | Get full text |
| ISSN | 1664-3224 1664-3224 |
| DOI | 10.3389/fimmu.2022.928374 |
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| Abstract | HLA-DR3 (DR3) is one of the dominant HLA-DR alleles associated with systemic lupus erythematosus (SLE) susceptibility. Our previous studies showed multiple intramolecular DR3 restricted T cell epitopes in the Smith D (SmD) protein, from which we generated a non-homologous, bacterial epitope mimics library. From this library we identified ABC
247-261
Mimic as one new DR3 restricted bacterial T cell epitope from the ABC transporter ATP-binding protein in
Clostridium tetani
. It activated and induced autoreactive SmD
66-80
-specific T cells and induced autoantibodies to lupus-related autoantigens
in vivo
. Compared to healthy donors, SLE patients have a greater percentage of cross-reactive T cells to ABC
247-261
Mimic and SmD
66-80
. In addition, we analyzed the ability of single DR3 restricted Tetanus toxoid (TT) T cell epitopes to induce autoimmune T cells. We found that the immunodominant TT epitope TT
826-845
stimulated SmD
66-80
reactive T cells but failed to induce persistent anti-SmD autoantibodies compared to the ABC
247-261
Mimic. Thus, exposure to the ABC
247-261
Mimic epitope may contribute to autoimmunity in susceptible DR3 individuals. |
|---|---|
| AbstractList | HLA-DR3 (DR3) is one of the dominant HLA-DR alleles associated with systemic lupus erythematosus (SLE) susceptibility. Our previous studies showed multiple intramolecular DR3 restricted T cell epitopes in the Smith D (SmD) protein, from which we generated a non-homologous, bacterial epitope mimics library. From this library we identified ABC
247-261
Mimic as one new DR3 restricted bacterial T cell epitope from the ABC transporter ATP-binding protein in
Clostridium tetani
. It activated and induced autoreactive SmD
66-80
-specific T cells and induced autoantibodies to lupus-related autoantigens
in vivo
. Compared to healthy donors, SLE patients have a greater percentage of cross-reactive T cells to ABC
247-261
Mimic and SmD
66-80
. In addition, we analyzed the ability of single DR3 restricted Tetanus toxoid (TT) T cell epitopes to induce autoimmune T cells. We found that the immunodominant TT epitope TT
826-845
stimulated SmD
66-80
reactive T cells but failed to induce persistent anti-SmD autoantibodies compared to the ABC
247-261
Mimic. Thus, exposure to the ABC
247-261
Mimic epitope may contribute to autoimmunity in susceptible DR3 individuals. HLA-DR3 (DR3) is one of the dominant HLA-DR alleles associated with systemic lupus erythematosus (SLE) susceptibility. Our previous studies showed multiple intramolecular DR3 restricted T cell epitopes in the Smith D (SmD) protein, from which we generated a non-homologous, bacterial epitope mimics library. From this library we identified ABC247-261 Mimic as one new DR3 restricted bacterial T cell epitope from the ABC transporter ATP-binding protein in Clostridium tetani. It activated and induced autoreactive SmD66-80-specific T cells and induced autoantibodies to lupus-related autoantigens in vivo. Compared to healthy donors, SLE patients have a greater percentage of cross-reactive T cells to ABC247-261 Mimic and SmD66-80. In addition, we analyzed the ability of single DR3 restricted Tetanus toxoid (TT) T cell epitopes to induce autoimmune T cells. We found that the immunodominant TT epitope TT826-845 stimulated SmD66-80 reactive T cells but failed to induce persistent anti-SmD autoantibodies compared to the ABC247-261 Mimic. Thus, exposure to the ABC247-261 Mimic epitope may contribute to autoimmunity in susceptible DR3 individuals.HLA-DR3 (DR3) is one of the dominant HLA-DR alleles associated with systemic lupus erythematosus (SLE) susceptibility. Our previous studies showed multiple intramolecular DR3 restricted T cell epitopes in the Smith D (SmD) protein, from which we generated a non-homologous, bacterial epitope mimics library. From this library we identified ABC247-261 Mimic as one new DR3 restricted bacterial T cell epitope from the ABC transporter ATP-binding protein in Clostridium tetani. It activated and induced autoreactive SmD66-80-specific T cells and induced autoantibodies to lupus-related autoantigens in vivo. Compared to healthy donors, SLE patients have a greater percentage of cross-reactive T cells to ABC247-261 Mimic and SmD66-80. In addition, we analyzed the ability of single DR3 restricted Tetanus toxoid (TT) T cell epitopes to induce autoimmune T cells. We found that the immunodominant TT epitope TT826-845 stimulated SmD66-80 reactive T cells but failed to induce persistent anti-SmD autoantibodies compared to the ABC247-261 Mimic. Thus, exposure to the ABC247-261 Mimic epitope may contribute to autoimmunity in susceptible DR3 individuals. HLA-DR3 (DR3) is one of the dominant HLA-DR alleles associated with systemic lupus erythematosus (SLE) susceptibility. Our previous studies showed multiple intramolecular DR3 restricted T cell epitopes in the Smith D (SmD) protein, from which we generated a non-homologous, bacterial epitope mimics library. From this library we identified ABC Mimic as one new DR3 restricted bacterial T cell epitope from the ABC transporter ATP-binding protein in . It activated and induced autoreactive SmD -specific T cells and induced autoantibodies to lupus-related autoantigens . Compared to healthy donors, SLE patients have a greater percentage of cross-reactive T cells to ABC Mimic and SmD . In addition, we analyzed the ability of single DR3 restricted Tetanus toxoid (TT) T cell epitopes to induce autoimmune T cells. We found that the immunodominant TT epitope TT stimulated SmD reactive T cells but failed to induce persistent anti-SmD autoantibodies compared to the ABC Mimic. Thus, exposure to the ABC Mimic epitope may contribute to autoimmunity in susceptible DR3 individuals. HLA-DR3 (DR3) is one of the dominant HLA-DR alleles associated with systemic lupus erythematosus (SLE) susceptibility. Our previous studies showed multiple intramolecular DR3 restricted T cell epitopes in the Smith D (SmD) protein, from which we generated a non-homologous, bacterial epitope mimics library. From this library we identified ABC247-261 Mimic as one new DR3 restricted bacterial T cell epitope from the ABC transporter ATP-binding protein in Clostridium tetani. It activated and induced autoreactive SmD66-80-specific T cells and induced autoantibodies to lupus-related autoantigens in vivo. Compared to healthy donors, SLE patients have a greater percentage of cross-reactive T cells to ABC247-261 Mimic and SmD66-80. In addition, we analyzed the ability of single DR3 restricted Tetanus toxoid (TT) T cell epitopes to induce autoimmune T cells. We found that the immunodominant TT epitope TT826-845 stimulated SmD66-80 reactive T cells but failed to induce persistent anti-SmD autoantibodies compared to the ABC247-261 Mimic. Thus, exposure to the ABC247-261 Mimic epitope may contribute to autoimmunity in susceptible DR3 individuals. |
| Author | Fu, Shu Man Gaskin, Felicia Kannapell, Carol C. Kwok, William W. Zhao, Zhenhuan Anderson, Ashley N. |
| AuthorAffiliation | 1 Division of Rheumatology, Department of Medicine, University of Virginia , Charlottesville, VA , United States 2 Center for Immunity, Inflammation and Regenerative Medicine, Division of Nephrology, Department of Medicine, University of Virginia , Charlottesville, VA , United States 3 Benaroya Research Institute, Virginia Mason , Seattle, WA , United States 4 Department of Psychiatry and Neurobehavioral Sciences, University of Virginia , Charlottesville, VA , United States |
| AuthorAffiliation_xml | – name: 1 Division of Rheumatology, Department of Medicine, University of Virginia , Charlottesville, VA , United States – name: 3 Benaroya Research Institute, Virginia Mason , Seattle, WA , United States – name: 2 Center for Immunity, Inflammation and Regenerative Medicine, Division of Nephrology, Department of Medicine, University of Virginia , Charlottesville, VA , United States – name: 4 Department of Psychiatry and Neurobehavioral Sciences, University of Virginia , Charlottesville, VA , United States |
| Author_xml | – sequence: 1 givenname: Zhenhuan surname: Zhao fullname: Zhao, Zhenhuan – sequence: 2 givenname: Ashley N. surname: Anderson fullname: Anderson, Ashley N. – sequence: 3 givenname: Carol C. surname: Kannapell fullname: Kannapell, Carol C. – sequence: 4 givenname: William W. surname: Kwok fullname: Kwok, William W. – sequence: 5 givenname: Felicia surname: Gaskin fullname: Gaskin, Felicia – sequence: 6 givenname: Shu Man surname: Fu fullname: Fu, Shu Man |
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| Cites_doi | 10.1056/NEJMoa021933 10.1084/jem.189.3.531 10.1371/journal.pone.0169086 10.4049/jimmunol.1800904 10.1016/j.molimm.2013.01.012 10.1002/ana.410390213 10.1016/j.jaut.2011.05.004 10.1172/jci8476 10.1038/ncomms7681 10.1073/pnas.1311861110 10.1385/1-59259-291-0:143 10.1056/nejmra1100359 10.1093/intimm/dxm099 10.1016/j.jaut.2011.07.002 10.1126/scitranslmed.aan2306 10.1016/j.jneuroim.2009.11.006 10.1016/j.chom.2019.05.003 10.4049/jimmunol.176.5.2781 10.1002/0471142735.im0314s24 10.4049/jimmunol.0902670 10.1002/art.40930 10.1007/s10067-010-1373-y 10.1007/s12026-016-8822-x 10.1007/s001250051373 10.1093/intimm/12.6.747 10.1136/annrheumdis-2018-214125 10.4049/jimmunol.168.10.5326 10.1177/0961203309345732 10.1186/s12865-020-00357-w 10.1201/9781315533247 10.1016/j.clim.2014.02.004 10.1084/jem.184.3.1167 10.1186/s12974-015-0313-9 10.4049/jimmunol.1501073 10.1007/s12016-011-8294-7 10.1073/pnas.1424796112 10.1136/lupus-2016-000199 10.3389/fimmu.2018.02811 |
| ContentType | Journal Article |
| Copyright | Copyright © 2022 Zhao, Anderson, Kannapell, Kwok, Gaskin and Fu. Copyright © 2022 Zhao, Anderson, Kannapell, Kwok, Gaskin and Fu 2022 Zhao, Anderson, Kannapell, Kwok, Gaskin and Fu |
| Copyright_xml | – notice: Copyright © 2022 Zhao, Anderson, Kannapell, Kwok, Gaskin and Fu. – notice: Copyright © 2022 Zhao, Anderson, Kannapell, Kwok, Gaskin and Fu 2022 Zhao, Anderson, Kannapell, Kwok, Gaskin and Fu |
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| Keywords | molecular mimicry systemic lupus erythematosus (SLE) cross-reactive T cells T cell epitope environmental bacteria Smith D (SmD) autoantigen HLA-DR3 |
| Language | English |
| License | Copyright © 2022 Zhao, Anderson, Kannapell, Kwok, Gaskin and Fu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Diego Francisco Catalán, University of Chile, Chile Reviewed by: Ricardo Pujol Borrell, Universitat Autònoma de Barcelona, Spain; Katina Schinnerling, University of Chile, Chile This article was submitted to Autoimmune and Autoinflammatory Disorders, a section of the journal Frontiers in Immunology |
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| SubjectTerms | Autoantibodies autoantigen Autoantigens Clostridium tetani environmental bacteria Epitopes, T-Lymphocyte HLA-DR3 HLA-DR3 Antigen Humans Immunology Lupus Erythematosus, Systemic molecular mimicry Smith D (SmD) T cell epitope T-Lymphocytes |
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| Title | HLA-DR3 restricted environmental epitopes from the bacterium Clostridium tetani have T cell cross-reactivity to the SLE-related autoantigen SmD |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/36389825 https://www.proquest.com/docview/2737468979 https://pubmed.ncbi.nlm.nih.gov/PMC9659850 https://doaj.org/article/8a5387e845c1455892485b2493883d1b |
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