Journal ArticleDOI
A leading role for the immune system in the pathophysiology of preeclampsia
TLDR
The pathophysiology of preeclampsia may involve several factors, including persistent hypoxia at the placental level and the release of high amounts of STBMs, which may contribute to the inflammatory process and to changes in adaptive‐immune system cells, which are also modulated in preeclamping.Abstract:
Preeclampsia syndrome is characterized by inadequate placentation, because of deficient trophoblastic invasion of the uterine spiral arteries, leading to placental hypoxia, secretion of proinflammatory cytokines, the release of angiogenic and antiangiogenic factors and miRNAs. Although immune-system alterations are associated with the origin of preeclampsia, other factors, including proinflammatory cytokines, neutrophil activation, and endothelial dysfunction, are also related to the pathophysiology of this syndrome. The pathophysiology of preeclampsia may involve several factors, including persistent hypoxia at the placental level and the release of high amounts of STBMs. DAMP molecules released under hypoxic conditions and STBMs, which bind TLRs, may activate monocytes, DCs, NK cells, and neutrophils, promoting persistent inflammatory conditions in this syndrome. The development of hypertension in preeclamptic women is also associated with endothelial dysfunction, which may be mediated by various mechanisms, including neutrophil activation and NET formation. Furthermore, preeclamptic women have higher levels of nonclassic and intermediate monocytes and lower levels of lymphoid BDCA-2(+) DCs. The cytokines secreted by these cells may contribute to the inflammatory process and to changes in adaptive-immune system cells, which are also modulated in preeclampsia. The changes in T cell subsets that may be seen in preeclampsia include low Treg activity, a shift toward Th1 responses, and the presence of Th17 lymphocytes. B cells can participate in the pathophysiology of preeclampsia by producing autoantibodies against adrenoreceptors and autoantibodies that bind the AT1-R.read more
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Journal ArticleDOI
Immunological Tolerance, Pregnancy, and Preeclampsia: The Roles of Semen Microbes and the Father.
Louise C. Kenny,Douglas B. Kell +1 more
TL;DR: Overall, it is argued for a significant paternal role in the development of PE through microbial infection of the mother via insemination through microbes from the gut, oral and female urinary tract microbiomes as the main sources of the infection.
Journal ArticleDOI
Placental Galectins Are Key Players in Regulating the Maternal Adaptive Immune Response.
Andrea Balogh,Eszter Tóth,Roberto Romero,Katalin Paréj,Diana Csala,Nikolett L. Szenasi,István Hajdú,Kata Juhasz,Árpád Kovács,Hamutal Meiri,Petronella Hupuczi,Adi L. Tarca,Adi L. Tarca,Adi L. Tarca,Sonia S. Hassan,Sonia S. Hassan,Offer Erez,Péter Závodszky,János Matkó,Zoltán Papp,Simona W. Rossi,Sinuhe Hahn,Éva Pállinger,Nandor Gabor Than,Nandor Gabor Than +24 more
TL;DR: Results show that Gal-13 and Gal-14 already provide an immunoprivileged environment at the maternal-fetal interface during early pregnancy, and their reduced expression is related to miscarriages.
Journal ArticleDOI
Angiotensin II-induced hypertension and cardiac hypertrophy are differentially mediated by TLR3- and TLR4-dependent pathways.
Madhu V. Singh,Michael Z. Cicha,Sarah Nunez,David K. Meyerholz,Mark W. Chapleau,Mark W. Chapleau,Francois M. Abboud +6 more
TL;DR: It is concluded that Angiotensin II activates both TLR4-TRIF and TLR3- TRIF pathways in a nonredundant manner whereby hypertension is dependent on activation of the TLR 3-TR IF pathway and cardiac hypertrophy is dependent upon both TLr3-TRif and TLr4-trIF pathways.
Journal ArticleDOI
Sex differences in T cells in hypertension.
TL;DR: Novel therapeutic targets need to be identified in both sexes to increase the percentage of hypertensive individuals with controlled BP and how the different components of the immune system interact so that specific mechanisms can be targeted therapeutically without compromising natural immune defenses.
Journal ArticleDOI
Lnc-DC mediates the over-maturation of decidual dendritic cells and induces the increase in Th1 cells in preeclampsia
Wen Zhang,Yang Zhou,YiLing Ding +2 more
TL;DR: Preeclampsia is a severe pregnancy‐related disease that involves an imbalance of the immune reaction, which is dominated by T helper1 (Th1) cells; however, the mechanism is unclear.
References
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Journal ArticleDOI
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Journal ArticleDOI
Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia
Sharon Maynard,Jiang Yong Min,Jaime R. Merchan,Kee-Hak Lim,Jianyi Li,Susanta Mondal,Towia A. Libermann,James P. Morgan,Frank W. Sellke,Isaac E. Stillman,Franklin H. Epstein,Vikas P. Sukhatme,S. Ananth Karumanchi +12 more
TL;DR: It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia.
Journal ArticleDOI
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Journal ArticleDOI
Circulating Angiogenic Factors and the Risk of Preeclampsia
Richard J. Levine,Sharon Maynard,Cong Qian,Kee-Hak Lim,Lucinda England,Kai F. Yu,Enrique F. Schisterman,Ravi Thadhani,Benjamin P. Sachs,Franklin H. Epstein,Bahaeddine M Sibai,Vikas P. Sukhatme,S. Ananth Karumanchi +12 more
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