Evidence map›Paper›PMID 35602884›Full record

ArticleClinical & translational immunology2022

G-CSF induces CD15

Ebtehag Maneta, Livingstone Fultang, Jemma Taylor, Matthew Pugh, William Jenkinson, Graham Anderson, Arri Coomarasamy, Mark D Kilby, David M Lissauer, Francis Mussai and 1 more

Open access · goldAbstract read
In one paragraph

Article in Clinical & translational immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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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

11 authors at 4 institutions in 2 countries.

Ebtehag ManetaInstitute of Immunology and Immunotherapy University of Birmingham Birmingham UK.
Livingstone FultangInstitute of Immunology and Immunotherapy University of Birmingham Birmingham UK.
Jemma TaylorInstitute of Immunology and Immunotherapy University of Birmingham Birmingham UK.
Matthew PughInstitute of Immunology and Immunotherapy University of Birmingham Birmingham UK.ORCID https://orcid.org/0000-0002-6324-661X
William JenkinsonInstitute of Immunology and Immunotherapy University of Birmingham Birmingham UK.
Graham AndersonInstitute of Immunology and Immunotherapy University of Birmingham Birmingham UK.
Arri CoomarasamyTommy's National Centre for Miscarriage Research Institute of Metabolism and Systems Research University of Birmingham Birmingham UK.
Mark D KilbyInstitute of Metabolism and Systems Research University of Birmingham Birmingham UK.
David M LissauerInstitute of Life Course and Medical Sciences University of Liverpool Liverpool UK.
Francis MussaiInstitute of Immunology and Immunotherapy University of Birmingham Birmingham UK.ORCID https://orcid.org/0000-0003-3342-0047
Carmela De SantoInstitute of Immunology and Immunotherapy University of Birmingham Birmingham UK.
University of Birmingham · GBChildren’s Foundation · GBMiscarriage Association · GBUniversity of Liverpool · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Recombinant granulocyte colony-stimulating factor (G-CSF) is frequently administered to patients with cancer to enhance granulocyte recovery post-chemotherapy. Clinical trials have also used G-CSF to modulate myeloid cell function in pregnancy and inflammatory diseases. Although the contribution of G-CSF to expanding normal granulocytes is well known, the effect of this cytokine on the phenotype and function of immunosuppressive granulocytic cells remains unclear. Here, we investigate the impact of physiological and iatrogenic G-CSF on an as yet undescribed granulocyte phenotype and ensuing outcome on T cells in the settings of cancer and pregnancy. Methods: Granulocytes from patients treated with recombinant G-CSF, patients with late-stage cancer and women enrolled on a trial of recombinant G-CSF were phenotyped by flow cytometry. The ability and mechanism of polarised granulocytes to suppress T-cell proliferation were assessed by cell proliferation assays, flow cytometry and ELISA. Results: We observed that G-CSF leads to a significant upregulation of CD14 expression on CD15 Conclusions: G-CSF induces a population of ROS

Indexed as

cancerCD15+CD14+G‐CSFMDSCplacenta

Identifiers

PMID35602884
PMCPMC9114661
OpenAlexW4285291978

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.