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Interleukin 10-2849AA genotype protects against pre-eclampsia

Genes & Immunity volume 5, pages 313–314 (2004)Cite this article

Abstract

Recently, it has been described that human fertility is associated with the interleukin 10 (IL10) −2849 AA genotype. Pre-eclampsia is the most common pregnancy-specific complication. In the pathogenesis of pre-eclampsia, IL10 may affect maternal intravascular inflammation as well as endothelial dysfunction. Therefore, we tested the hypothesis that pre-eclampsia is associated with genetic variation in the IL10 promoter region in a case–control study for pre-eclampsia. Women homozygous for the IL10 −2849A allele have a threefold reduced risk for pre-eclampsia compared to controls (odds ratio 0.29; 95% CI 0.10–0.83). No differences in genotype frequency were found for polymorphisms in the IL10 promoter region at positions −1082, −819 and −592. This suggests that there is a genetically determined mechanism which protects the mother against pre-eclampsia, as reflected in the lower frequency of the IL10 −2849AA genotype in pre-eclamptic women.

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Author notes

  1. C J M de Groot: CJM de Groot is supported by the Netherlands Organisation for Scientific Research (NWO)

Authors and Affiliations

  1. Department of Obstetrics and Gynecology, Erasmus Medical Center Rotterdam, The Netherlands

    C J M de Groot & M W J C Jansen

  2. Department of Hematology, Leiden University Medical Center, Leiden, The Netherlands

    R M Bertina

  3. Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands

    J J M Schonkeren & T W J Huizinga

  4. Department of Obstetrics, Gynecology and Reproductive Medicine, Leiden University Medical Center, Leiden, The Netherlands

    F M Helmerhorst

Authors
  1. C J M de Groot
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  2. M W J C Jansen
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  3. R M Bertina
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  4. J J M Schonkeren
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  5. F M Helmerhorst
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  6. T W J Huizinga
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Correspondence to C J M de Groot.

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de Groot, C., Jansen, M., Bertina, R. et al. Interleukin 10-2849AA genotype protects against pre-eclampsia. Genes Immun 5, 313–314 (2004). https://doi.org/10.1038/sj.gene.6364092

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  • DOI: https://doi.org/10.1038/sj.gene.6364092

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