Ethnicity Authors The year of publication The experimental group The control group Samples Conclusions British Hiby et al. [64 ] 2004 PE patients ( Full-term pregnant women ( Mothers: blood The combination of maternal KIR AA and fetal HLA-C2 was more common in PE. Japanese Saito et al. [65 ] 2006 Couples with Japanese women and Caucasian men ( 2003 database in Japan ( — There was no statistical difference in the incidence of PE between the two groups. White British Hiby et al. [20 ] 2010 PE patients ( Normal primiparas ( Mothers: blood Maternal KIR AA was related to PE when the fetus had more HLA-C2 inherited from the father. Maternal telomeric KIR B (KIR2DS1) was a protective factor for PE. Mexico Sánchez-Rodríguez et al. [37 ] 2011 PE patients ( Normal pregnant women ( Mothers: decidual samples PE patients tended to have more inhibitory KIRs. Chinese Han population Yu et al. [70 ] 2014 PE patients ( Normal pregnant women ( Mothers and fathers: blood Less PE patients had KIR2DS1, and more PE patients had AA genotype compared with normal pregnant women. More PE patients with KIR AA had fewer HLA-C2 than their babies. Chinese Han population Long et al. [72 ] 2014 PE patients ( Normal pregnant women ( Mothers: blood PE patients had less activating KIRs (2DS2, 2DS3, and 2DS5). The frequency of KIR2DL1 was increased in PE patients when the neonate was HLA-C2C2. Uganda (sub-Saharan Africans) Nakimuli et al. [68 ] 2015 PE patients ( Normal pregnant women ( Mothers: blood The combination of maternal KIR AA and fetal HLA-C2 was related with PE. KIR2DS5 and KIR2DL1 had the protective effect on PE. European Johnsen et al. [73 ] 2018 PE patients ( Normal pregnant women ( Mothers: blood, decidua, or muscle PE patients with acute atherosis tended to have the combination of maternal KIR-B and fetal HLA-C2 compared with PE patients without acute atherosis. European Larsen et al. [74 ] 2019 Severe PE patients ( Normal pregnant women ( Mothers: blood There was no effect of KIR/HLA-C combination on the risk of severe PE.
