IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v5y2014i1d10.1038_ncomms4359.html
   My bibliography  Save this article

MHC-dependent inhibition of uterine NK cells impedes fetal growth and decidual vascular remodelling

Author

Listed:
  • Jens Kieckbusch

    (University of Cambridge School of Clinical Medicine, NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital
    Centre for Trophoblast Research, University of Cambridge)

  • Louise M. Gaynor

    (University of Cambridge School of Clinical Medicine, NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital
    Centre for Trophoblast Research, University of Cambridge)

  • Ashley Moffett

    (Centre for Trophoblast Research, University of Cambridge
    University of Cambridge)

  • Francesco Colucci

    (University of Cambridge School of Clinical Medicine, NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital
    Centre for Trophoblast Research, University of Cambridge)

Abstract

NK cells express variable receptors that engage polymorphic MHC class I molecules and regulate their function. Maternal NK cells accumulate at the maternal-fetal interface and can interact with MHC class I molecules from both parents. The relative contribution of the two sets of parental MHC molecules to uterine NK cell function is unknown. Here we show that, in mice, maternal and not paternal MHC educates uterine NK cells to mature and acquire functional competence. The presence of an additional MHC allele that binds more inhibitory than activating NK cell receptors results in suppressed NK cell function, compromised uterine arterial remodelling and reduced fetal growth. Notably, reduced fetal growth occurs irrespectively of the parental origin of the inhibitory MHC. This provides biological evidence for the impact of MHC-dependent NK inhibition as a risk factor for human pregnancy-related complications associated with impaired arterial remodelling.

Suggested Citation

  • Jens Kieckbusch & Louise M. Gaynor & Ashley Moffett & Francesco Colucci, 2014. "MHC-dependent inhibition of uterine NK cells impedes fetal growth and decidual vascular remodelling," Nature Communications, Nature, vol. 5(1), pages 1-13, May.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4359
    DOI: 10.1038/ncomms4359
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms4359
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms4359?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Mengwei Han & Luni Hu & Di Wu & Yime Zhang & Peng Li & Xingyu Zhao & Yanyu Zeng & Guanqun Ren & Zhiyuan Hou & Yanli Pang & Tongbiao Zhao & Chao Zhong, 2023. "IL-21R-STAT3 signalling initiates a differentiation program in uterine tissue-resident NK cells to support pregnancy," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4359. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.