Evidence map›Paper›PMID 42637745›Full record

ArticleNature communications2026

ACKR2 aids the regulation of bone marrow eosinophils to promote monocyte differentiation and anti-bacterial immunity.

Gillian J Wilson, Lily Koumbas Foley, Zuzanna Pocalun, Elise Pitmon, Ayumi Fukuoka, Kit M Lee, Lauren Fernandez, Heather Mathie, Robin Bartolini, Laura Medina-Ruiz and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Gillian J WilsonChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK. gillian.wilson@glasgow.ac.uk.ORCID http://orcid.org/0000-0002-9513-8437
Lily Koumbas FoleyChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.ORCID http://orcid.org/0009-0004-8281-0791
Zuzanna PocalunChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.
Elise PitmonChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.
Ayumi FukuokaChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.ORCID http://orcid.org/0000-0002-6752-7814
Kit M LeeChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.
Lauren FernandezChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.ORCID http://orcid.org/0009-0002-8805-9340
Heather MathieChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.ORCID http://orcid.org/0000-0002-0444-3306
Robin BartoliniChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.ORCID http://orcid.org/0000-0001-6875-6734
Laura Medina-RuizChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.
John J ColeChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK.
Gerard J GrahamChemokine Research Group, School of Infection and Immunity, University of Glasgow, Glasgow, UK. gerard.graham@glasgow.ac.uk.ORCID http://orcid.org/0000-0002-7801-204X

Funding

RCUK | Medical Research Council (MRC) MR/V010972/1Wellcome TrustWellcome Trust (Wellcome) 217093/Z/19/Z
6 · The paper itself

Abstract

Chemokine receptors control cell migration within the body. Here we reveal interactions between eosinophils and monocytes in the bone marrow, indirectly controlled by the atypical chemokine receptor ACKR2. In the absence of ACKR2, there are decreased numbers of eosinophils in the bone marrow. As a result, eosinophil and monocyte interactions are reduced within the bone marrow niche, and are associated with changes in monocyte gene expression. Monocytes from ACKR2-/- mice are recruited to the tissues but are fundamentally altered in their ability to differentiate into macrophages, in the lung, peritoneal cavity and cavity wall. Bacterial elimination is impaired in ACKR2-/- mice during peritoneal infection. ACKR2 is therefore a key regulator of eosinophil-driven monocyte education in the bone marrow, required for full monocyte differentiation and macrophage function within the tissues.

Indexed as

Bone Marrow CellsCell DifferentiationEosinophilsMonocytesReceptors, ChemokineAnimalsBone MarrowCell MovementChemokine Receptor D6MacrophagesMiceMice, Inbred C57BLMice, KnockoutAckr2 protein, mouseChemokine Receptor D6Receptors, Chemokine

Identifiers

PMID42637745
PMCPMC13503710

What OpenQuestion holds

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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.