ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Involvement of T-Helper 9 Activation in a Mouse Model of Allergic Rhinitis.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Th9 and IL9 in Chronic Superior Airway Inflammation: A Narrative Review.Biomedicines · 2026Review
- Role of LINC00240 on T-helper 9 differentiation in allergic rhinitis through influencing DNMT1-dependent methylation of PU.1.Immunologic research · 2024Article
- Recent advances in understanding the effects of T lymphocytes on mucosal barrier function in allergic rhinitis.Frontiers in immunology · 2023Review
- T Helper 9 Cells: A New Player in Immune-Related Diseases.DNA and cell biology · 2019Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND We aimed to investigate the role of T-Helper (TH) 9 cells in the pathogenesis of allergic rhinitis (AR) in mice. MATERIAL AND METHODS An AR model was produced in BALB/c mice, and the viral encoding interleukin (IL)-9 silencing sequence was used to reduce IL-9 expression. The experiment was divided into a control group, an AR group, an IL-9 shRNA+AR group, and a vector+AR group. Hematoxylin and eosin (H&E) staining was used to detect pathological changes. The cytokine expression was detected by ELISA method. Cellular typing was detected by flow cytometry. RESULTS Cells in the control group were regularly arranged, with clear layers and no congestion, edema, or necrosis observable. By contrast, in the AR model group and the vector treatment group, nasal mucosa showed clear hyperemia and edema in upper tissues and infiltration of inflammatory cells, which were ameliorated by IL-9 silencing. Compared with the control group, interferon-γ (IFN-γ) was significantly down-regulated, while IL-4, IL-17, and IL-9 were significantly elevated in the AR model group. TH1 cells in nasal mucosa, lymph, nasal lavage, spleen, and peripheral blood were significantly reduced, while TH2, TH9, TH17, and Treg cells were significantly elevated in the AR group compared with the control group. Importantly, all these changes in AR model were ameliorated by IL-9 silencing. CONCLUSIONS AR is related to the changes of cytokines in TH1, TH2, TH9, TH17, and Treg, which are improved by IL-9 silencing. Activation of TH9 cells is involved in the pathogenesis of AR.
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Registered trials
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