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MiR‐29b regulates Th2 cell differentiation in asthma by targeting inducible B7‐H3 and STAT3

BACKGROUND: MicroRNAs play an important role in T cell responses. However, how microRNAs regulate Th cells in asthma remains poorly defined. OBJECTIVE: In this study, we investigated the mechanism and pathways of miR‐29b regulating Th cells in asthma, in order to find new targets for asthma. METHODS...

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Autores principales: Gu, Wenjing, Li, Gang, Zhang, Weili, Zhang, Xinxing, He, Yanyu, Huang, Li, Yan, Yongdong, Ji, Wei, Hao, Chuangli, Chen, Zhengrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8764737/
https://www.ncbi.nlm.nih.gov/pubmed/35079347
http://dx.doi.org/10.1002/clt2.12114
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author Gu, Wenjing
Li, Gang
Zhang, Weili
Zhang, Xinxing
He, Yanyu
Huang, Li
Yan, Yongdong
Ji, Wei
Hao, Chuangli
Chen, Zhengrong
author_facet Gu, Wenjing
Li, Gang
Zhang, Weili
Zhang, Xinxing
He, Yanyu
Huang, Li
Yan, Yongdong
Ji, Wei
Hao, Chuangli
Chen, Zhengrong
author_sort Gu, Wenjing
collection PubMed
description BACKGROUND: MicroRNAs play an important role in T cell responses. However, how microRNAs regulate Th cells in asthma remains poorly defined. OBJECTIVE: In this study, we investigated the mechanism and pathways of miR‐29b regulating Th cells in asthma, in order to find new targets for asthma. METHODS: We detected miR‐29b, B7‐H3 and STAT3 in the peripheral blood of children with asthma, explored the relationship between these molecules and their effects on T cells through in vitro cell culture, and verified it by animal model. RESULTS: MiR‐29b levels were decreased in the peripheral blood mononuclear cells from children with asthma. Vitro studies found that the expression of miR‐29b in macrophages was decreased and the expression of B7‐H3 and STAT3 was increased after house dust mite (HDM) stimulation. After down‐regulation of miR‐29b in macrophages, the expressions of B7‐H3 and STAT3 in macrophages were increased and T cells differentiate into Th2 cells. After the addition of B7‐H3 or STAT3 antibodies, the differentiation of naive T cells into Th2 cells was reduced. In OVA induced mice asthmatic model, after the up‐regulation of miR‐29b in lung, the expression of B7‐H3 and STAT3 decreased in the lung tissues of mice, and the expression of Th2 cells and type II cytokine decreased simultaneously. The pathological changes of lung tissues were also alleviated. CONCLUSION: The expression of miR‐29b is decreased in asthmatic children. MiR‐29b can inhibit Th2 cell differentiation by inhibiting B7‐H3 and STAT3 pathways at the same time, and reduce asthmatic immune inflammation.
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spelling pubmed-87647372022-01-24 MiR‐29b regulates Th2 cell differentiation in asthma by targeting inducible B7‐H3 and STAT3 Gu, Wenjing Li, Gang Zhang, Weili Zhang, Xinxing He, Yanyu Huang, Li Yan, Yongdong Ji, Wei Hao, Chuangli Chen, Zhengrong Clin Transl Allergy Original Article BACKGROUND: MicroRNAs play an important role in T cell responses. However, how microRNAs regulate Th cells in asthma remains poorly defined. OBJECTIVE: In this study, we investigated the mechanism and pathways of miR‐29b regulating Th cells in asthma, in order to find new targets for asthma. METHODS: We detected miR‐29b, B7‐H3 and STAT3 in the peripheral blood of children with asthma, explored the relationship between these molecules and their effects on T cells through in vitro cell culture, and verified it by animal model. RESULTS: MiR‐29b levels were decreased in the peripheral blood mononuclear cells from children with asthma. Vitro studies found that the expression of miR‐29b in macrophages was decreased and the expression of B7‐H3 and STAT3 was increased after house dust mite (HDM) stimulation. After down‐regulation of miR‐29b in macrophages, the expressions of B7‐H3 and STAT3 in macrophages were increased and T cells differentiate into Th2 cells. After the addition of B7‐H3 or STAT3 antibodies, the differentiation of naive T cells into Th2 cells was reduced. In OVA induced mice asthmatic model, after the up‐regulation of miR‐29b in lung, the expression of B7‐H3 and STAT3 decreased in the lung tissues of mice, and the expression of Th2 cells and type II cytokine decreased simultaneously. The pathological changes of lung tissues were also alleviated. CONCLUSION: The expression of miR‐29b is decreased in asthmatic children. MiR‐29b can inhibit Th2 cell differentiation by inhibiting B7‐H3 and STAT3 pathways at the same time, and reduce asthmatic immune inflammation. John Wiley and Sons Inc. 2022-01-18 /pmc/articles/PMC8764737/ /pubmed/35079347 http://dx.doi.org/10.1002/clt2.12114 Text en © 2022 The Authors. Clinical and Translational Allergy published by John Wiley & Sons Ltd on behalf of European Academy of Allergy and Clinical Immunology. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Gu, Wenjing
Li, Gang
Zhang, Weili
Zhang, Xinxing
He, Yanyu
Huang, Li
Yan, Yongdong
Ji, Wei
Hao, Chuangli
Chen, Zhengrong
MiR‐29b regulates Th2 cell differentiation in asthma by targeting inducible B7‐H3 and STAT3
title MiR‐29b regulates Th2 cell differentiation in asthma by targeting inducible B7‐H3 and STAT3
title_full MiR‐29b regulates Th2 cell differentiation in asthma by targeting inducible B7‐H3 and STAT3
title_fullStr MiR‐29b regulates Th2 cell differentiation in asthma by targeting inducible B7‐H3 and STAT3
title_full_unstemmed MiR‐29b regulates Th2 cell differentiation in asthma by targeting inducible B7‐H3 and STAT3
title_short MiR‐29b regulates Th2 cell differentiation in asthma by targeting inducible B7‐H3 and STAT3
title_sort mir‐29b regulates th2 cell differentiation in asthma by targeting inducible b7‐h3 and stat3
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8764737/
https://www.ncbi.nlm.nih.gov/pubmed/35079347
http://dx.doi.org/10.1002/clt2.12114
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