期刊
PLACENTA
卷 75, 期 -, 页码 27-33出版社
W B SAUNDERS CO LTD
DOI: 10.1016/j.placenta.2018.11.008
关键词
Pregnancy; Preeclampsia; HLA; KIR; NK cells
资金
- Region Zealand Health Sciences Research Foundation
- Zealand University Hospital
- Danish National Research Foundation
- Pharmacy Foundation
- Egmont Foundation
- March of Dimes Birth Defects Foundation
- Health Foundation
- Novo Nordisk Foundation
- Lundbeck Foundation
- Danish Medical Research Council
- Innovation Fund Denmark
- Nordea Foundation
- Aarhus Ideas
- University of Copenhagen Strategic Grant
- Danish Council for Independent Research
Introduction: The pathogenesis of preeclampsia may involve inadequate trophoblast invasion caused by excessive inhibition of uterine natural killer cells (uNK) by extravillous trophoblast cells (EVT). This may be the result of a combination of maternal killer-cell immunoglobin-like receptor (KIR) AA genotype and fetal human leukocyte antigen-C2 (HLA-C2) genotype. A few studies have reported a significantly increased frequency of the maternal KIR AA/fetal HLA-C2 combination in cases of preeclampsia compared to controls. Methods: Study subjects were 259 cases of severe preeclampsia/eclampsia and 259 matched pregnant women without preeclampsia or eclampsia. All pregnancies were singleton pregnancies, and mothers were preferentially primigravidae. Blood samples from women and their newborns were obtained from the Danish National Birth Cohort (DNBC) and the Danish Neonatal Screening Biobank. Significant differences in the frequencies of KIR AA and HLA-C2 between cases and controls were investigated. Results: No significant difference was observed between cases and controls in the frequency of maternal KIR AA (OR=0.86, 95% CI=0.60-1.23, P=0.41), neither when the fetus carried an HLA-C2 allele (OR=0.85, 95% CI=0.52-1.38, P=0.51), nor when the fetus carried an HLA-C2 allele more than its mother (OR=0.75, 95% CI=0.34-1.64, P=0.47). Conclusion: The Results show no influence of HLA-C/KIR genetic variation on the risk of severe preeclampsia, contrary to what some previous studies have observed. An explanation could be that severe preeclampsia represents a separate pathological entity compared to mild preeclampsia.
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