Disruption in the regulation of immune responses in the placental subtype of preeclampsia

dc.contributor.authorGeldenhuys, Janri
dc.contributor.authorRossouw, Theresa M.
dc.contributor.authorLombaard, Hendrik Andries
dc.contributor.authorEhlers, Marthie Magdaleen
dc.contributor.authorKock, Marleen M.
dc.contributor.emailmarleen.kock@up.ac.zaen_ZA
dc.date.accessioned2019-03-13T15:00:43Z
dc.date.available2019-03-13T15:00:43Z
dc.date.issued2018-07-20
dc.description.abstractPreeclampsia is a pregnancy-specific disorder, of which one of its major subtypes, the placental subtype is considered a response to an ischemic placental environment, impacting fetal growth and pregnancy outcome. Inflammatory immune responses have been linked to metabolic and inflammatory disorders as well as reproductive failures. In healthy pregnancy, immune regulatory mechanisms prevent excessive systemic inflammation. However, in preeclampsia, the regulation of immune responses is disrupted as a result of aberrant activation of innate immune cells and imbalanced differentiation of T-helper cell subsets creating a cytotoxic environment in utero. Recognition events that facilitate immune interaction between maternal decidual T cells, NK cells, and cytotrophoblasts are considered an indirect cause of the incomplete remodeling of spiral arteries in preeclampsia. The mechanisms involved include the activation of immune cells and the subsequent secretion of cytokines and placental growth factors affecting trophoblast invasion, angiogenesis, and eventually placentation. In this review, we focus on the role of excessive systemic inflammation as the result of a dysregulated immune system in the development of preeclampsia. These include insufficient control of inflammation, failure of tolerance toward paternal antigens at the fetal–maternal interface, and subsequent over- or insufficient activation of immune mediators. It is also possible that external stimuli, such as bacterial endotoxin, may contribute to the excessive systemic inflammation in preeclampsia by stimulating the release of pro-inflammatory cytokines. In conclusion, a disrupted immune system might be a predisposing factor or result of placental oxidative stress or excessive inflammation in preeclampsia. Preeclampsia can thus be considered a hyperinflammatory state associated with defective regulation of the immune system proposed as a key element in the pathological events of the placental subtype of this disorder.en_ZA
dc.description.departmentImmunologyen_ZA
dc.description.departmentMedical Microbiologyen_ZA
dc.description.librarianam2019en_ZA
dc.description.sponsorshipThe University of Pretoria, the National Health Laboratory Service (NHLS), and the National Research Foundation (NRF)en_ZA
dc.description.urihttp://www.frontiersin.org/Immunologyen_ZA
dc.identifier.citationGeldenhuys J, Rossouw TM, Lombaard HA, Ehlers MM and Kock MM (2018) Disruption in the Regulation of Immune Responses in the Placental Subtype of Preeclampsia. Front. Immunol. 9:1659. DOI: 10.3389/fimmu.2018.01659.en_ZA
dc.identifier.issn1664-3224 (online)
dc.identifier.other10.3389/fimmu.2018.01659
dc.identifier.urihttp://hdl.handle.net/2263/68651
dc.language.isoenen_ZA
dc.publisherFrontiers Mediaen_ZA
dc.rights© 2018 Authors. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).en_ZA
dc.subjectPreeclampsiaen_ZA
dc.subjectTrophoblast invasionen_ZA
dc.subjectImmune regulationen_ZA
dc.subjectPregnancyen_ZA
dc.subjectMonocytesen_ZA
dc.subjectInflammationen_ZA
dc.subjectNatural killer cellsen_ZA
dc.subjectEndothelial growth factoren_ZA
dc.subjectFetal–maternal interfaceen_ZA
dc.subjectNecrosis-factor-alphaen_ZA
dc.subjectEndovascular trophoblast invasionen_ZA
dc.subjectDecidual NK cellsen_ZA
dc.subjectT cellsen_ZA
dc.subjectAngiogenic factorsen_ZA
dc.subjectPeripheral blood (PB)en_ZA
dc.subjectEarly pregnancyen_ZA
dc.titleDisruption in the regulation of immune responses in the placental subtype of preeclampsiaen_ZA
dc.typeArticleen_ZA

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