期刊
BIOMEDICINES
卷 8, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/biomedicines8060162
关键词
antiphospholipid syndrome; antiphospholipid antibodies; estradiol; tissue factor; monocytes; in vitro
资金
- internal grant agency of Palacky University [IGA UP_2020_016, IGA UP_2020_002]
- Ministry of Health of the Czech Republic (MH CZ-DRO) [00098892]
- State Committee Science MES RA [SCS 18T-1F396]
Antiphospholipid syndrome (APS) is the most common cause of acquired thrombophilia and recurrent spontaneous miscarriages associated with extended persistence of antiphospholipid antibodies (aPL). How circulating aPL and high-17 beta-estradiol (E2) environment contribute to the pregnancy complications in APS is poorly defined. Therefore, we aimed to analyse whether E2 could be responsible for the immune cell hyperactivation in aPL- positive (lupus anticoagulant, anti-cardiolipin, anti-beta 2-glycoprotein) in women. For this, peripheral blood mononuclear cells (PBMCs) from 14 aPL- positive and 13 aPL- negative women were cultured in the presence or absence of E2, LPS or E2+LPS and cell immunophenotype and cytokine release were analysed. In the aPL+ group, E2 presence markedly increased the percentage of NK cells positive for CD69 (p< 0.05), monocytes positive for tissue factor (TF, CD142) (p< 0.05), and B cells expressing PD-L1 (p< 0.05), as well as the elevated production of IL-1 beta comparing to aPL- women (p< 0.01). Regardless of aPL positivity, E2 augmented the procoagulatory response elicited by LPS in monocytes. Our findings show the ability of E2 to promote proinflammatory and procoagulatory phenotype of innate immune cells in individuals with aPL positivity. Our data highlights the significant impact of female hormones on the activation of immune cells in the presence of aPL.
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