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Published on: August 13, 2019
17beta-Estradiol utilizes the estrogen receptor to regulate CD16 expression in monocytes
P R Kramer1, V Winger, S F Kramer
1Department of Biomedical Sciences, Baylor College of Dentistry, Texas A&M University Health Science Center, 3302 Gaston Avenue, Dallas, TX 75246, USA. pkramer@bcd.tamhsc.edu
Molecular and Cellular Endocrinology
|October 10, 2007
Summary
Estrogen reduces CD16 expression and cytokine release in monocytes, a process mediated by estrogen receptors (ERalpha and ERbeta). Fulvestrant blocks this effect, and ERalpha directly interacts with the CD16 promoter.
Area of Science:
- Immunology
- Endocrinology
- Molecular Biology
Background:
- Estrogen influences immune cell function, including CD16 expression and cytokine release.
- The specific roles of estrogen receptor (ER) alpha and beta in regulating CD16 expression in monocytes are not fully understood.
Purpose of the Study:
- To investigate the involvement of ERalpha and ERbeta in estrogen-mediated regulation of CD16 expression and subsequent cytokine release in monocytic cells.
- To elucidate the molecular mechanisms by which estrogen affects CD16 transcription.
Main Methods:
- Monocytic cells were treated with 17beta-estradiol and ER antagonists/agonists.
- CD16 transcript levels, TNF-alpha and IL-1beta release were measured.
- Chromatin immunoprecipitation and luciferase reporter assays were used to assess ER-promoter interactions and transcriptional activity.
Main Results:
- Estrogen significantly decreased CD16 transcript levels and TNF-alpha/IL-1beta release upon CD16 activation, an effect blocked by fulvestrant.
- ERalpha was found to interact with a region 5' of the CD16 gene, indicating a direct role in transcriptional regulation.
- Both ERalpha and ERbeta agonists reduced CD16 reporter gene expression, suggesting involvement of both receptor subtypes.
Conclusions:
- Estrogen, acting through ERalpha and ERbeta, downregulates CD16 expression in monocytic cells.
- ERalpha directly binds to the CD16 promoter, influencing its transcription.
- These findings reveal a novel mechanism of immune modulation by estrogen via CD16 regulation.
