ArticleClinical and experimental immunology2019
Mitigating placental injuries through up-regulating DAF in experimental APS mice: new mechanism of progesterone.
Article in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Toxoplasma gondii infection reduces CD59 expression through downregulation of JAK2/STAT3 signaling axis to enhance decidual NK cell cytotoxicity via the RAS/MAPK pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Coagulation parameter-based nomogram for the diagnosis of obstetric antiphospholipid syndrome and its subtypes.Open life sciences · 2026Article
- Immune-mediated mechanisms and maternal-fetal interface dysfunction in obstetric antiphospholipid syndrome.Frontiers in immunology · 2025Review
- ARID5B-mediated LINC01128 epigenetically activated pyroptosis and apoptosis by promoting the formation of the BTF3/STAT3 complex in β2GPI/anti-β2GPI-treated monocytes.Clinical and translational medicine · 2024Article
- Inactivation of Yes-Associated Protein Mediates Trophoblast Dysfunction: A New Mechanism of Pregnancy Loss Associated with Anti-Phospholipid Antibodies?Biomedicines · 2022Article
- Protection by hydroxychloroquine prevents placental injury in obstetric antiphospholipid syndrome.Journal of cellular and molecular medicine · 2022Article
- Sex-Specific Causal Relations between Steroid Hormones and Obesity-A Mendelian Randomization Study.Metabolites · 2021Article
- The immunology of the fetal-placental unit comes of age.Clinical and experimental immunology · 2019Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-phospholipid syndrome (APS) is characterized by recurrent pathological pregnancy, arterial or venous thrombosis in the presence of anti-phospholipid antibody (aPL). Complement activation is recognized as an intermediate link leading to placental thrombosis and placental inflammation in APS model mice. Decay accelerating factor (DAF, CD55), MAC-inhibitory protein (MAC-IP, CD59) and membrane co-factor protein (MCP, CD46) are important complement inhibitory proteins (CIPs) highly expressed in normal placenta to curb excessive complement activation and its mediated injuries. Anti-β2 glycoprotein I (anti-β2GPI) antibody is an important aPL. We found that placental DAF and CD46 decreased in β2GPI passively immunized APS model mice, accompanied by C3 deposition, neutrophil infiltration and increased proinflammatory cytokine levels detected in its placenta. Progesterone supplement can up-regulate DAF but not CD46 expression, curb C3 activation and decrease proinflammatory cytokines levels to reduce fetal loss frequency. Progesterone receptor antagonist (mifepristone) or knock-down DAF with specific siRNA, above the protective effects of progesterone, were significantly weakened. Another sex hormone, oestrogen, has no significant effect on placental DAF and C3 contents and fetal loss frequency in the APS mice model. This may be an important mechanism by which progesterone induces maternal-fetal immune tolerance. At the same time, it may provide evidence for the use of progesterone in APS abortion patients.
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