Academic Journal
Estrogen Receptor Alpha Gene (ESR1) Facilitates Th2-immune Response and Enhances Th2 Cytokines in Experimental Atopic Dermatitis Mice
العنوان: | Estrogen Receptor Alpha Gene (ESR1) Facilitates Th2-immune Response and Enhances Th2 Cytokines in Experimental Atopic Dermatitis Mice |
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المؤلفون: | Jianrong Niu, Hui Zhou, Rong Tian, Xudong Wang |
المصدر: | Iranian Journal of Immunology, Vol 20, Iss 2, Pp 167-176 (2023) |
بيانات النشر: | Shiraz University of Medical Sciences, 2023. |
سنة النشر: | 2023 |
المجموعة: | LCC:Biology (General) |
مصطلحات موضوعية: | antagonist, atopic dermatitis, esr1, inflammatory cytokines, mice, Biology (General), QH301-705.5 |
الوصف: | Background: Molecular markers are involved in atopic dermatitis (AD) pathogenesis. The estrogen receptor (ESR)-1 gene, encoding ERα, is reported to express aberrantly in AD patients.Objective: To detect the biological functions of ESR1 in 2,4 dinitrochlorobenzene (DNCB)-treated mice.Methods: The DNCB-treated mice received a topical application of emulsion containing the 1,3-bis(4 hydroxyphenyl)-4-methyl-5-[4-(2-piperidinyl ethoxy) phenol]-1H-pyrazole dihydrochloride (MPP; an ESR1-selective antagonist) to dorsal skins and ears. Then the dermatitis scores, histopathological changes, and cytokine levels were evaluated.Results: MPP specifically downregulated ESR1 expression in DNCB-applied mice. Functionally, application of MPP abolished the DNCB-induced promotion in dermatitis score. Additionally, MPP administration protected against DNCB-induced dermatitis severity, suppressed mast cell infiltration and reduced production of immunoglobulin E (IgE) and thymus and activation-regulated chemokine (TARC). Moreover, MPP treatment inhibited DNCB- induced production of Th2 cytokines and infiltration of CD4+ T cells.Conclusion: ESR1 facilitates Th2-immune response and enhances Th2 cytokines in AD mice. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1735-1383 1735-367X |
Relation: | https://iji.sums.ac.ir/article_49308_75a0c1dbc99a8103f3930b8053d19f1c.pdf; https://doaj.org/toc/1735-1383; https://doaj.org/toc/1735-367X |
DOI: | 10.22034/iji.2023.97283.2494 |
URL الوصول: | https://doaj.org/article/912a4cdf05104a6887b93f65b591b3dd |
رقم الانضمام: | edsdoj.912a4cdf05104a6887b93f65b591b3dd |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 17351383 1735367X |
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DOI: | 10.22034/iji.2023.97283.2494 |