PMID- 35845477
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220719
IS  - 2305-5839 (Print)
IS  - 2305-5847 (Electronic)
IS  - 2305-5839 (Linking)
VI  - 10
IP  - 12
DP  - 2022 Jun
TI  - Narrative review of the relationship between the maternal-fetal interface immune 
      tolerance and the onset of preeclampsia.
PG  - 713
LID - 10.21037/atm-22-2287 [doi]
LID - 713
AB  - BACKGROUND AND OBJECTIVE: The establishment of maternal-fetal interface immune 
      tolerance is essential for successful pregnancy. Studies have shown that 
      spontaneous abortion, recurrent abortion, and fetal growth restriction are 
      related to maternal-fetal interface immune dysfunction. Preeclampsia is an 
      idiopathic condition related to pregnancy which manifests as hypertension, 
      proteinuria, and other target organ damage after 20 weeks of gestation. Although 
      the etiology of preeclampsia is still unknown, its pathogenesis is thought to be 
      related to genetics, environment, and metabolism. In recent years, more and more 
      studies have been conducted on the mechanism of immune tolerance at the 
      maternal-fetal interface and the relationship between immune dysregulation and 
      the pathogenesis of preeclampsia. This paper summarizes the latest studies on 
      this topic in order to find new insights into the pathogenesis of preeclampsia 
      and make a reflection on clinical diagnosis and treatment in different phenotype 
      of preeclampsia. METHODS: The research and latest progress published from 2000 to 
      December 2021 on the relationship between maternal-fetal interface immune 
      tolerance and preeclampsia were broadly retrieved and researched using PubMed and 
      Web of Science databases. KEY CONTENT AND FINDINGS: The mechanism of natural 
      killer cells (NK cells) and macrophages at the maternal-fetal interface in immune 
      tolerance, as well as their cytotoxicity and cytokine secretion dysfunction, may 
      be related to the pathogenesis of preeclampsia. The expression of nonclassical 
      type I human leukocyte antigen (HLA) on extravillous trophoblast (EVT) cell were 
      down-regulated in decidua of preeclampsia, which may induce increase EVT death 
      caused by activating of cytotoxic NK cell. In addition, genetic polymorphism of 
      nonclassical type I HLA on the EVT cell membrane may be related to the 
      pathogenesis of preeclampsia, although this is likely to be a combination of 3 
      nonclassical type I HLA genotypes and requires sequencing to verify. CONCLUSIONS: 
      We demonstrated how the maternal-fetal interface immune dysfunction contribute to 
      the pathogenesis of preeclampsia, further study and clinical trial based on this 
      theory of pathogenesis may reveal new immune treatment method of preeclampsia.
CI  - 2022 Annals of Translational Medicine. All rights reserved.
FAU - Luo, Fangyuan
AU  - Luo F
AD  - Department of Obstetrics and Gynecology, Sichuan Provincial People's Hospital, 
      University of Electronic Science and Technology of China, Chengdu, China.
AD  - Department of Obstetrics and Gynecology, West China Second University Hospital of 
      Sichuan University, Chengdu, China.
FAU - Yue, Jun
AU  - Yue J
AD  - Department of Obstetrics and Gynecology, Sichuan Provincial People's Hospital, 
      University of Electronic Science and Technology of China, Chengdu, China.
FAU - Li, Lingling
AU  - Li L
AD  - Department of Obstetrics and Gynecology, Sichuan Provincial People's Hospital, 
      University of Electronic Science and Technology of China, Chengdu, China.
FAU - Mei, Jie
AU  - Mei J
AD  - Department of Obstetrics and Gynecology, Sichuan Provincial People's Hospital, 
      University of Electronic Science and Technology of China, Chengdu, China.
FAU - Liu, Xinghui
AU  - Liu X
AD  - Department of Obstetrics and Gynecology, West China Second University Hospital of 
      Sichuan University, Chengdu, China.
FAU - Huang, Yu
AU  - Huang Y
AD  - Department of Obstetrics and Gynecology, Sichuan Provincial People's Hospital, 
      University of Electronic Science and Technology of China, Chengdu, China.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - China
TA  - Ann Transl Med
JT  - Annals of translational medicine
JID - 101617978
PMC - PMC9279811
OTO - NOTNLM
OT  - Immunity
OT  - human leukocyte antigen (HLA)
OT  - maternal-fetal interface
OT  - natural killer cells (NK cells)
OT  - preeclampsia
COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure 
      form (available at 
      https://atm.amegroups.com/article/view/10.21037/atm-22-2287/coif). The authors 
      have no conflicts of interest to declare.
EDAT- 2022/07/19 06:00
MHDA- 2022/07/19 06:01
PMCR- 2022/06/01
CRDT- 2022/07/18 03:50
PHST- 2022/04/13 00:00 [received]
PHST- 2022/06/14 00:00 [accepted]
PHST- 2022/07/18 03:50 [entrez]
PHST- 2022/07/19 06:00 [pubmed]
PHST- 2022/07/19 06:01 [medline]
PHST- 2022/06/01 00:00 [pmc-release]
AID - atm-10-12-713 [pii]
AID - 10.21037/atm-22-2287 [doi]
PST - ppublish
SO  - Ann Transl Med. 2022 Jun;10(12):713. doi: 10.21037/atm-22-2287.