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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Public Library of Science (PLoS)
2021-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0249605&type=printable |
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| author | Carolin Boehne Ann-Kathrin Behrendt Almut Meyer-Bahlburg Martin Boettcher Sebastian Drube Thomas Kamradt Gesine Hansen |
| author_facet | Carolin Boehne Ann-Kathrin Behrendt Almut Meyer-Bahlburg Martin Boettcher Sebastian Drube Thomas Kamradt Gesine Hansen |
| author_sort | Carolin Boehne |
| collection | DOAJ |
| 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. |
| format | Article |
| id | doaj-art-8d7d5a930fd44214b3c4c38a50f8694e |
| institution | DOAJ |
| issn | 1932-6203 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-8d7d5a930fd44214b3c4c38a50f8694e2025-08-20T02:54:31ZengPublic Library of Science (PLoS)PLoS ONE1932-62032021-01-01164e024960510.1371/journal.pone.0249605Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma.Carolin BoehneAnn-Kathrin BehrendtAlmut Meyer-BahlburgMartin BoettcherSebastian DrubeThomas KamradtGesine HansenT 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.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0249605&type=printable |
| spellingShingle | Carolin Boehne Ann-Kathrin Behrendt Almut Meyer-Bahlburg Martin Boettcher Sebastian Drube Thomas Kamradt Gesine Hansen Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma. PLoS ONE |
| 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 |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0249605&type=printable |
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