Format

Send to

Choose Destination
Immunol Invest. 2014;43(5):424-35. doi: 10.3109/08820139.2013.879173. Epub 2014 Feb 24.

The variations in the IL1RL1 gene and susceptibility to preeclampsia.

Author information

1
Department of Forensic Biology, West China School of Preclinical and Forensic Medicine, Sichuan University , Chengdu 610041 , P.R. China .

Abstract

The IL1RL1, which encodes at least three isoforms by alternative splicing, has been identified to be involved in the initiation and perpetuation of inflammation. In spite of being a main contributor of maternal and perinatal mortality, the mechanism responsible for the pathophysiology of preeclampsia has not yet been well addressed. To investigate the relationship between IL1RL1 polymorphisms and preeclampsia risk, we identified the correlation between three tag SNPs (rs13017455, rs1420103 and rs17027006) in IL1RL1 with preeclampsia risk in a case-control study. A total of 214 cases and 208 controls were recruited to participate in this study. Genotypes of the three SNPs were determined with the use of polymerase chain reaction-restriction fragment length polymorphism assay. Significantly reduced preeclampsia risk was found to be associated with the CT genotype of rs13017455 (p = 0. 032, OR = 0. 66, 95% CI = 0.45-0.97) in overdominant model. Differences were particularly significant in the severe preeclampsia subgroup (p = 0.045, OR = 0.66, 95% CI = 0.44-0.99) and the early-onset severe preeclampsia subgroup (p = 0.0097, OR = 0.47, 95% CI = 0.26-0.84). Significantly increased mild preeclampsia risk was observed associated with GG genotype of rs1420103 polymorphisms (p = 0.029, OR = 2.18, 95% CI = 1.09-4.34), while reducing late-onset severe preeclampsia susceptibility was associated with TT genotype of rs1420103 (p = 0.02, OR = 0.49, 95% CI = 0.26-0.92).

KEYWORDS:

Association; IL1RL1; polymorphisms; preeclampsia

PMID:
24564816
DOI:
10.3109/08820139.2013.879173
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Taylor & Francis
Loading ...
Support Center