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Interferon Genes Are Influenced by 17β-Estradiol in SLE
Ram P Singh1,2, Bevra H Hahn2, David S Bischoff1,3
1Research Service, Veteran Administration Greater Los Angeles Healthcare System, Los Angeles, CA, United States.
Frontiers in Immunology
|November 4, 2021
Summary
The female hormone 17β-estradiol promotes inflammation in Systemic Lupus Erythematosus (SLE) by increasing pro-inflammatory cytokines and interferon-stimulated genes, impacting T cells via ERα.
Area of Science:
- Immunology
- Endocrinology
- Molecular Biology
Background:
- Systemic Lupus Erythematosus (SLE) exhibits a known link between inflammation and 17β-estradiol, affecting immune cells and autoantibodies.
- The precise molecular mechanisms by which estradiol influences SLE pathogenesis, particularly its impact on target genes and pathways, remain incompletely understood.
- Previous research indicated elevated estradiol levels in female SLE patients compared to healthy individuals.
Purpose of the Study:
- To investigate the effects of 17β-estradiol on the expression of interferon-stimulated genes (ISGs) and pro-inflammatory cytokines/chemokines.
- To explore the correlation between estradiol levels, specific cytokine levels, and disease activity in SLE patients.
- To elucidate the role of estradiol and its receptor (ERα) in modulating immune cell activation and cytokine production.
Main Methods:
- Analysis of interferon-stimulated genes and pro-inflammatory cytokines/chemokines in response to 17β-estradiol treatment.
- Measurement of plasma cytokine levels (IL-6, IL-12, IL-17, IL-18, SCF, IL-21/IL-23) and correlation with 17β-estradiol levels and SLE disease activity index (SLEDAI).
- In vitro treatment of peripheral blood mononuclear cells (PBMCs) from SLE patients and healthy controls with 17β-estradiol and an ERα inhibitor, followed by assessment of cytokine secretion and T cell populations (CD3+CD69+, CD3+IFNγ+).
Main Results:
- Significant 5-10-fold increase in interferon-regulated genes in healthy females treated with 17β-estradiol.
- Elevated plasma levels of IL-6, IL-12, IL-17, IL-18, SCF, and IL-21/IL-23 in SLE patients, correlating positively with 17β-estradiol levels.
- 17β-estradiol treatment in vitro increased pro-inflammatory cytokines/chemokines and activated T cells (CD3+CD69+, CD3+IFNγ+), an effect blocked by an ERα inhibitor.
Conclusions:
- 17β-estradiol significantly upregulates interferon-stimulated genes and pro-inflammatory cytokines/chemokines.
- Estradiol levels correlate with increased cytokine production and disease activity in SLE patients.
- The findings highlight 17β-estradiol's role in SLE pathogenesis via ERα-mediated induction of inflammatory responses.
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