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Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma

T cell immunoglobulin and mucin domain-containing molecule-3 (Tim-3) has been described as a transmembrane protein, expressed on the surface of various T cells as well as different cells of innate immunity. It has since been associated with Th1 mediated autoimmune diseases and transplantation tolera...

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Autores principales: Boehne, Carolin, Behrendt, Ann-Kathrin, Meyer-Bahlburg, Almut, Boettcher, Martin, Drube, Sebastian, Kamradt, Thomas, Hansen, Gesine
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8023500/
https://www.ncbi.nlm.nih.gov/pubmed/33822811
http://dx.doi.org/10.1371/journal.pone.0249605
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author Boehne, Carolin
Behrendt, Ann-Kathrin
Meyer-Bahlburg, Almut
Boettcher, Martin
Drube, Sebastian
Kamradt, Thomas
Hansen, Gesine
author_facet Boehne, Carolin
Behrendt, Ann-Kathrin
Meyer-Bahlburg, Almut
Boettcher, Martin
Drube, Sebastian
Kamradt, Thomas
Hansen, Gesine
author_sort Boehne, Carolin
collection PubMed
description T cell immunoglobulin and mucin domain-containing molecule-3 (Tim-3) has been described as a transmembrane protein, expressed on the surface of various T cells as well as different cells of innate immunity. It has since been associated with Th1 mediated autoimmune diseases and transplantation tolerance studies, thereby indicating a possible role of this receptor in counter-regulation of Th2 immune responses. In the present study we therefore directly examined the role of Tim-3 in allergic inflammation and respiratory tolerance. First, Tim-3(-/-) mice and wild type controls were immunized and challenged with the model allergen ovalbumin (OVA) to induce an asthma-like phenotype. Analysis of cell numbers and distribution in the bronchoalveolar lavage (BAL) fluid as well as lung histology in H&E stained lung sections demonstrated a comparable degree of eosinophilic inflammation in both mouse strains. Th2 cytokine production in restimulated cell culture supernatants and serum IgE and IgG levels were equally increased in both genotypes. In addition, cell proliferation and the distribution of different T cell subsets were comparable. Moreover, analysis of both mouse strains in our respiratory tolerance model, where mucosal application of the model allergen before immunization, prevents the development of an asthma-like phenotype, revealed no differences in any of the parameters mentioned above. The current study demonstrates that Tim-3 is dispensable not only for the development of allergic inflammation but also for induction of respiratory tolerance in mice in an OVA-based model.
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spelling pubmed-80235002021-04-15 Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma Boehne, Carolin Behrendt, Ann-Kathrin Meyer-Bahlburg, Almut Boettcher, Martin Drube, Sebastian Kamradt, Thomas Hansen, Gesine PLoS One Research Article T cell immunoglobulin and mucin domain-containing molecule-3 (Tim-3) has been described as a transmembrane protein, expressed on the surface of various T cells as well as different cells of innate immunity. It has since been associated with Th1 mediated autoimmune diseases and transplantation tolerance studies, thereby indicating a possible role of this receptor in counter-regulation of Th2 immune responses. In the present study we therefore directly examined the role of Tim-3 in allergic inflammation and respiratory tolerance. First, Tim-3(-/-) mice and wild type controls were immunized and challenged with the model allergen ovalbumin (OVA) to induce an asthma-like phenotype. Analysis of cell numbers and distribution in the bronchoalveolar lavage (BAL) fluid as well as lung histology in H&E stained lung sections demonstrated a comparable degree of eosinophilic inflammation in both mouse strains. Th2 cytokine production in restimulated cell culture supernatants and serum IgE and IgG levels were equally increased in both genotypes. In addition, cell proliferation and the distribution of different T cell subsets were comparable. Moreover, analysis of both mouse strains in our respiratory tolerance model, where mucosal application of the model allergen before immunization, prevents the development of an asthma-like phenotype, revealed no differences in any of the parameters mentioned above. The current study demonstrates that Tim-3 is dispensable not only for the development of allergic inflammation but also for induction of respiratory tolerance in mice in an OVA-based model. Public Library of Science 2021-04-06 /pmc/articles/PMC8023500/ /pubmed/33822811 http://dx.doi.org/10.1371/journal.pone.0249605 Text en © 2021 Boehne et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Boehne, Carolin
Behrendt, Ann-Kathrin
Meyer-Bahlburg, Almut
Boettcher, Martin
Drube, Sebastian
Kamradt, Thomas
Hansen, Gesine
Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma
title Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma
title_full Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma
title_fullStr Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma
title_full_unstemmed Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma
title_short Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma
title_sort tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8023500/
https://www.ncbi.nlm.nih.gov/pubmed/33822811
http://dx.doi.org/10.1371/journal.pone.0249605
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