Human leukocyte antigen HLA-C, HLA-G, HLA-F, and HLA-E placental profiles are altered in early severe preeclampsia and preterm birth with chorioamnionitis.


Journal

American journal of obstetrics and gynecology
ISSN: 1097-6868
Titre abrégé: Am J Obstet Gynecol
Pays: United States
ID NLM: 0370476

Informations de publication

Date de publication:
10 2022
Historique:
received: 07 03 2022
revised: 11 07 2022
accepted: 13 07 2022
pubmed: 22 7 2022
medline: 5 10 2022
entrez: 21 7 2022
Statut: ppublish

Résumé

The extravillous trophoblast expresses each of the nonclassical major histocompatibility complex class I antigens-human leukocyte antigens E, F, and G-and a single classical class I antigen, human leukocyte antigen C. We recently demonstrated dynamic expression patterns of human leukocyte antigens C, G, and F during early extravillous trophoblast invasion and placentation. This study aimed to investigate the hypothesis that the immune inflammatory mediated complications of pregnancy such as early preeclampsia and preterm labor may show altered expression profiles of nonclassical human leukocyte antigens. Real-time quantitative polymerase chain reaction, western blot, and immunohistochemistry were performed on placental villous tissues and basal plate sections from term nonlaboring deliveries, preterm deliveries, and severe early-onset preeclampsia, both with and without small-for-gestational-age neonates. Human leukocyte antigen G is strongly and exclusively expressed by the extravillous trophoblast within the placental basal plate, and its levels increase in pregnancies complicated by severe early-onset preeclampsia with small-for-gestational-age neonates relative to those of healthy term controls. Human leukocyte antigen C shows a similar profile in the extravillous trophoblast of preeclamptic pregnancies, but significantly decreases in the villous placenta. Human leukocyte antigen F protein levels are decreased in both extravillous trophoblast and villous placenta of severe early-onset preeclamptic pregnancies, both with and without small-for-gestational-age neonates, compared with those found in term and preterm birth deliveries. Human leukocyte antigen E decreases in blood vessels in placentas from preeclamptic pregnancies relative to its levels in term and preterm birth deliveries. Placental levels of human leukocyte antigens F and C are increased in cases of preterm birth with chorioamnionitis relative to those of cases of idiopathic preterm birth. Dysregulation of placental human leukocyte antigen expression at the maternal-fetal interface may contribute to compromised maternal tolerance in preterm birth with chorioamnionitis and excessive maternal systemic inflammation associated with severe early-onset preeclampsia.

Sections du résumé

BACKGROUND
The extravillous trophoblast expresses each of the nonclassical major histocompatibility complex class I antigens-human leukocyte antigens E, F, and G-and a single classical class I antigen, human leukocyte antigen C. We recently demonstrated dynamic expression patterns of human leukocyte antigens C, G, and F during early extravillous trophoblast invasion and placentation.
OBJECTIVE
This study aimed to investigate the hypothesis that the immune inflammatory mediated complications of pregnancy such as early preeclampsia and preterm labor may show altered expression profiles of nonclassical human leukocyte antigens.
STUDY DESIGN
Real-time quantitative polymerase chain reaction, western blot, and immunohistochemistry were performed on placental villous tissues and basal plate sections from term nonlaboring deliveries, preterm deliveries, and severe early-onset preeclampsia, both with and without small-for-gestational-age neonates.
RESULTS
Human leukocyte antigen G is strongly and exclusively expressed by the extravillous trophoblast within the placental basal plate, and its levels increase in pregnancies complicated by severe early-onset preeclampsia with small-for-gestational-age neonates relative to those of healthy term controls. Human leukocyte antigen C shows a similar profile in the extravillous trophoblast of preeclamptic pregnancies, but significantly decreases in the villous placenta. Human leukocyte antigen F protein levels are decreased in both extravillous trophoblast and villous placenta of severe early-onset preeclamptic pregnancies, both with and without small-for-gestational-age neonates, compared with those found in term and preterm birth deliveries. Human leukocyte antigen E decreases in blood vessels in placentas from preeclamptic pregnancies relative to its levels in term and preterm birth deliveries. Placental levels of human leukocyte antigens F and C are increased in cases of preterm birth with chorioamnionitis relative to those of cases of idiopathic preterm birth.
CONCLUSION
Dysregulation of placental human leukocyte antigen expression at the maternal-fetal interface may contribute to compromised maternal tolerance in preterm birth with chorioamnionitis and excessive maternal systemic inflammation associated with severe early-onset preeclampsia.

Identifiants

pubmed: 35863458
pii: S0002-9378(22)00575-0
doi: 10.1016/j.ajog.2022.07.021
pii:
doi:

Substances chimiques

HLA-C Antigens 0
HLA-F antigens 0
HLA-G Antigens 0
Histocompatibility Antigens Class I 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

641.e1-641.e13

Subventions

Organisme : CIHR
ID : FDN-143262
Pays : Canada

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Caroline E Dunk (CE)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Canada; Department of Experimental Therapeutics, Toronto General Hospital Research Institute, University Health Network, Toronto, Canada.

Matthew Bucher (M)

Department of Obstetrics and Gynecology, Oregon Health & Science University, Portland, OR.

Jianhong Zhang (J)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Canada.

Heyam Hayder (H)

Department of Biology, York University, Toronto, Canada.

Daniel E Geraghty (DE)

Fred Hutchinson Cancer Research Center, Seattle, WA.

Stephen J Lye (SJ)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Canada; Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Obstetrics and Gynecology, University of Toronto, Toronto, Canada; Department of Physiology, University of Toronto, Toronto, Canada.

Leslie Myatt (L)

Department of Obstetrics and Gynecology, Oregon Health & Science University, Portland, OR.

Rinat Hackmon (R)

Department of Obstetrics and Gynecology, Oregon Health & Science University, Portland, OR. Electronic address: hachmon@ohsu.edu.

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Classifications MeSH