Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

The paper, published in Nature Communications reveals key genes involved in the common developmental disease.

Artistic representation of early development. © Fugger Group
Artistic representation of early development.

Fetal growth restriction (FGR) is a serious global disease, affecting up to 10% of all pregnancies. It is one of the main reasons for disability, illness and death in newborn babies, and increases their risk of development delays as well as their future risk of heart disease, hypertension, type 2 diabetes and stroke in adult life. There is currently no cure for FGR and we do not have effective markers that can be used to screen or predict the likelihood of developing FGR in pregnancy.

A new study by researchers from the MRC Weatherall Institute of Molecular Medicine (MRC WIMM), University of Oxford and the Broad Institute of MIT and Harvard published in Nature Communications, demonstrates how certain combinations of parental and fetal immune genes lead to development of FGR in pregnancy.

This elegant study conducted at the Oxford Centre for Neuroinflammation led by Professor Lars Fugger at the MRC Human Immunology Unit in Oxford and in collaboration with Prof. Aviv Regev at the Broad Institute of MIT and Harvard, demonstrates how a discrete interaction between two immune genes leads to cellular crosstalk and transcriptional changes in a range of cell types at the maternal-fetal interface.

Dr Gurman Kaur (based at the MRC WIMM, Oxford and the Broad Institute of MIT and Harvard) in collaboration with Dr Caroline Porter (Broad Institute of MIT and Harvard) developed and employed a novel model system to show that products of two risk genes, the inhibitory KIR2DL1 receptor expressed on maternal uterine natural killer cells, and paternally-derived HLA-C*0501, an HLA-C group 2 allotype, expressed on fetal trophoblast cells, leads to FGR. The team employed cutting-edge technologies including single-cell technologies and micro-computated tomography imaging, and were able to show that the interaction between these genes leads to changes in the uterine spiral arteries that develop in pregnancy, providing a higher resistance to fetal blood flow in FGR.

The research provides a mechanistic understanding of FGR as a complex multicellular disease, and highlights gene candidates which have the potential to be modulated for therapeutic intervention, and improve clinical outcomes for both the mother and the baby.

Read the paper at Nature Communications

Similar stories

Biotech spinout MiroBio acquired by Gilead Sciences for ~£332m

Co-founded by Prof. Simon Davis, MiroBio focuses on developing therapeutics for inflammatory diseases.

Seven research groups secure LEAF Sustainability Awards

The Laboratory Efficiency Assessment Framework (LEAF) aims to support research groups to embed sustainability into their work.

Playful science at Wheatley and Holton Play and Activity Day 2022

On Saturday 16th July, volunteers from the MRC WIMM talked the science of blood, lab techniques and coding at the Play and Activity Day organised by the Oxfordshire Play Association.

Gold LEAF Award for Kusumbe Lab

The award demonstrates the group's commitment to sustainable science.

Novel all-in-one vaccine developed to tackle future coronavirus threats

Up to $30 million in funding has been announced by the Coalition for Epidemic Preparedness Innovations (CEPI) to bring a new nanoparticle vaccine offering protection against a range of coronaviruses to clinical trial.

Spatial transcriptomics of neurodegeneration in Progressive Multiple Sclerosis (MS)

In a paper published in Nature Neuroscience, the Fugger Group describe molecular pathways of MS neurodegeneration in unprecedented detail.