Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3
BackgroundAtopic dermatitis (AD), a common type 2 inflammatory disease, is driven by T helper (TH) 2/TH22polarization and cytokines.Galectin-9 (Gal-9), via its receptor T cell immunoglobulin- and mucin-domain-containing molecule-3 (TIM-3), can promote TH2/TH22 immunity. The relevance of this in AD i...
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| Format: | Article |
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Frontiers Media S.A.
2022-07-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2022.952338/full |
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| author | Wenxing Su Wenxing Su Wenxing Su Ji Zhang Shun Yang Minhui Tang Yu Shen Cuiping Liu Jiang Ji Marcus Maurer Marcus Maurer Qingqing Jiao |
| author_facet | Wenxing Su Wenxing Su Wenxing Su Ji Zhang Shun Yang Minhui Tang Yu Shen Cuiping Liu Jiang Ji Marcus Maurer Marcus Maurer Qingqing Jiao |
| author_sort | Wenxing Su |
| collection | DOAJ |
| description | BackgroundAtopic dermatitis (AD), a common type 2 inflammatory disease, is driven by T helper (TH) 2/TH22polarization and cytokines.Galectin-9 (Gal-9), via its receptor T cell immunoglobulin- and mucin-domain-containing molecule-3 (TIM-3), can promote TH2/TH22 immunity. The relevance of this in AD is largely unclear.ObjectivesTo characterize the role of TIM-3 and Gal-9 in the pathogenesis of AD and underlying mechanisms.MethodsWe assessed the expression of Gal-9 and TIM-3 in 30 AD patients, to compare them with those of 30 healthy controls (HC) and to explore possible links with disease features including AD activity (SCORAD), IgE levels, and circulating eosinophils and B cells. We also determined the effects of Gal-9 on T cells from the AD patients.ResultsOur AD patients had markedly higher levels of serum Gal-9 and circulating TIM-3-expressing TH1 and TH17 cells than HC. Gal-9 and TIM-3 were linked to high disease activity, IgE levels, and circulating eosinophils and/or B cells. The rates of circulating TIM-3-positive CD4+ cells were positively correlated with rates of TH2/TH22 cells and negatively correlated with rates of TH1/TH17 cells. Gal-9 inhibited the proliferation and induced the apoptosis of T cells in patients with AD, especially in those with severe AD.ConclusionOur findings suggest thatGal-9, via TIM-3, contributes to the pathogenesis of AD by augmenting TH2/TH22 polarization through the downregulation of TH1/TH17immunity. This makes Gal-9 and TIM-3 interesting to explore further, as possible drivers of disease and targets of novel AD treatment. |
| first_indexed | 2024-04-13T10:38:20Z |
| format | Article |
| id | doaj.art-9d8ea177554a4b8d82659cc5fef0986a |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-04-13T10:38:20Z |
| publishDate | 2022-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-9d8ea177554a4b8d82659cc5fef0986a2022-12-22T02:50:00ZengFrontiers Media S.A.Frontiers in Immunology1664-32242022-07-011310.3389/fimmu.2022.952338952338Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3Wenxing Su0Wenxing Su1Wenxing Su2Ji Zhang3Shun Yang4Minhui Tang5Yu Shen6Cuiping Liu7Jiang Ji8Marcus Maurer9Marcus Maurer10Qingqing Jiao11Department of Dermatology, The Second Affiliated Hospital of Soochow University, Su Zhou, ChinaDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, ChinaDepartment of Plastic and Burn Surgery, The Second Affiliated Hospital of Chengdu Medical College (China National Nuclear Corporation 416 Hospital), Chengdu, ChinaDepartment of Dermatology, The Second Affiliated Hospital of Soochow University, Su Zhou, ChinaDepartment of Dermatology, The Second Affiliated Hospital of Soochow University, Su Zhou, ChinaDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, ChinaJiangsu Institute of Clinical Immunology and Jiangsu Key Laboratory of Clinical Immunology, The First Affiliated Hospital of Soochow University, Suzhou, ChinaJiangsu Institute of Clinical Immunology and Jiangsu Key Laboratory of Clinical Immunology, The First Affiliated Hospital of Soochow University, Suzhou, ChinaDepartment of Dermatology, The Second Affiliated Hospital of Soochow University, Su Zhou, ChinaInstitute of Allergology, Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, GermanyAllergology and Immunology, Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, Berlin, GermanyDepartment of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, ChinaBackgroundAtopic dermatitis (AD), a common type 2 inflammatory disease, is driven by T helper (TH) 2/TH22polarization and cytokines.Galectin-9 (Gal-9), via its receptor T cell immunoglobulin- and mucin-domain-containing molecule-3 (TIM-3), can promote TH2/TH22 immunity. The relevance of this in AD is largely unclear.ObjectivesTo characterize the role of TIM-3 and Gal-9 in the pathogenesis of AD and underlying mechanisms.MethodsWe assessed the expression of Gal-9 and TIM-3 in 30 AD patients, to compare them with those of 30 healthy controls (HC) and to explore possible links with disease features including AD activity (SCORAD), IgE levels, and circulating eosinophils and B cells. We also determined the effects of Gal-9 on T cells from the AD patients.ResultsOur AD patients had markedly higher levels of serum Gal-9 and circulating TIM-3-expressing TH1 and TH17 cells than HC. Gal-9 and TIM-3 were linked to high disease activity, IgE levels, and circulating eosinophils and/or B cells. The rates of circulating TIM-3-positive CD4+ cells were positively correlated with rates of TH2/TH22 cells and negatively correlated with rates of TH1/TH17 cells. Gal-9 inhibited the proliferation and induced the apoptosis of T cells in patients with AD, especially in those with severe AD.ConclusionOur findings suggest thatGal-9, via TIM-3, contributes to the pathogenesis of AD by augmenting TH2/TH22 polarization through the downregulation of TH1/TH17immunity. This makes Gal-9 and TIM-3 interesting to explore further, as possible drivers of disease and targets of novel AD treatment.https://www.frontiersin.org/articles/10.3389/fimmu.2022.952338/fullT cell immunoglobulin- and mucin-domain-containing molecules-3 (TIM-3)Galectin-9 (Gal-9)TH1 cellsTH2 cellsTH17 cellsTH22 cells |
| spellingShingle | Wenxing Su Wenxing Su Wenxing Su Ji Zhang Shun Yang Minhui Tang Yu Shen Cuiping Liu Jiang Ji Marcus Maurer Marcus Maurer Qingqing Jiao Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3 Frontiers in Immunology T cell immunoglobulin- and mucin-domain-containing molecules-3 (TIM-3) Galectin-9 (Gal-9) TH1 cells TH2 cells TH17 cells TH22 cells |
| title | Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3 |
| title_full | Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3 |
| title_fullStr | Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3 |
| title_full_unstemmed | Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3 |
| title_short | Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3 |
| title_sort | galectin 9 contributes to the pathogenesis of atopic dermatitis via t cell immunoglobulin mucin 3 |
| topic | T cell immunoglobulin- and mucin-domain-containing molecules-3 (TIM-3) Galectin-9 (Gal-9) TH1 cells TH2 cells TH17 cells TH22 cells |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2022.952338/full |
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