Academic Journal

Estrogen Receptor Alpha Gene (ESR1) Facilitates Th2-immune Response and Enhances Th2 Cytokines in Experimental Atopic Dermatitis Mice

التفاصيل البيبلوغرافية
العنوان: Estrogen Receptor Alpha Gene (ESR1) Facilitates Th2-immune Response and Enhances Th2 Cytokines in Experimental Atopic Dermatitis Mice
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
الوصف
تدمد:17351383
1735367X
DOI:10.22034/iji.2023.97283.2494