Evidence map›Paper›PMID 31141500›Full record

ArticlePLoS biology2019

Placental chemokine compartmentalisation: A novel mammalian molecular control mechanism.

Kit Ming Lee, Gillian J Wilson, Marieke Pingen, Ayumi Fukuoka, Christopher A H Hansell, Robin Bartolini, Laura Medina-Ruiz, Gerard J Graham

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Kit Ming LeeChemokine Research Group, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0002-0475-3865
Gillian J WilsonChemokine Research Group, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0002-9513-8437
Marieke PingenChemokine Research Group, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0001-5689-9076
Ayumi FukuokaChemokine Research Group, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Christopher A H HansellChemokine Research Group, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Robin BartoliniChemokine Research Group, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Laura Medina-RuizChemokine Research Group, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0002-2934-534X
Gerard J GrahamChemokine Research Group, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.ORCID 0000-0002-7801-204X
University of Glasgow · GB

Funding

Medical Research Council MR/M019764/1Wellcome TrustWellcome Trust 9251/Z/12/Z
6 · The paper itself

Abstract

Atypical chemokine receptor 2 (ACKR2) is a chemokine-scavenging receptor. ACKR2-/-embryos display a reduction in size of a novel, to our knowledge, embryonic skin macrophage population referred to as 'intermediate' cells. CC chemokine receptor 2 (CCR2)-/-embryos display an identical phenotype, indicating that these cells require CCR2 to enable them to populate embryonic skin. Further analysis revealed that ACKR2-/-embryos have higher circulating concentrations of the CCR2 ligand, CC ligand 2 (CCL2); thus, ACKR2 regulates intraembryonic CCL2 levels. We show that ACKR2 is strongly expressed by trophoblasts and that it blocks movement of inflammatory chemokines, such as CCL2, from the maternal decidua into the embryonic circulation. We propose that trophoblastic ACKR2 is responsible for ensuring chemokine compartmentalisation on the maternal decidua, without which chemokines enter the embryonic circulation, disrupting gradients essential for directed intraembryonic cell migration. Overall, therefore, we describe a novel, to our knowledge, molecular mechanism whereby maternal decidual chemokines can function in a compartmentalised fashion without interfering with intraembryonic leukocyte migration. These data suggest similar functions for other atypical chemokine receptors in the placenta and indicate that defects in such receptors may have unanticipated developmental consequences.

Indexed as

AnimalsCell MovementChemokine Receptor D6ChemokinesDeciduaEmbryo, MammalianFemaleMacrophagesMammalsMice, Inbred C57BLMonocytesPlacentaPregnancyReceptors, ChemokineSkinTranscription, GeneticAckr2 protein, mouseChemokine Receptor D6ChemokinesReceptors, Chemokine

Identifiers

PMID31141500
PMCPMC6557524
OpenAlexW2947955848

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.