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Estrogen Receptor Alpha Gene (ESR1) Facilitates Th2-immune Response and Enhances Th2 Cytokines in Experimental Atopic Dermatitis Mice | ||
Iranian Journal of Immunology | ||
مقاله 3، دوره 20، شماره 2، شهریور 2023، صفحه 167-176 اصل مقاله (1.63 M) | ||
نوع مقاله: Original Article | ||
شناسه دیجیتال (DOI): 10.22034/iji.2023.97283.2494 | ||
نویسندگان | ||
Jianrong Niu1؛ Hui Zhou1؛ Rong Tian* 1؛ Xudong Wang2 | ||
1Department of Dermatology, Air Force Medical Center PLA, Beijing 100142, China. | ||
2Southern Medical District of Chinese PLA General Hospital, Beijing 100853, China. | ||
چکیده | ||
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. | ||
کلیدواژهها | ||
Antagonist؛ Atopic Dermatitis؛ ESR1؛ Inflammatory Cytokines؛ Mice | ||
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