Evidence map›Paper›PMID 32005854›Full record

ArticleScientific reports2020

Evaluation of the effect of GM-CSF blocking on the phenotype and function of human monocytes.

Noushin Lotfi, Guang-Xian Zhang, Nafiseh Esmaeil, Abdolmohamad Rostami

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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  7. Rethinking MS Therapeutics: From Disease Pathogenesis Mechanisms to AI-Driven Drug Discovery.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    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

4 authors at 2 institutions in 2 countries.

Noushin LotfiDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
Guang-Xian ZhangDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
Nafiseh EsmaeilDepartment of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. nafesm5@gmail.com.
Abdolmohamad RostamiDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA, USA. a.m.rostami@jefferson.edu.
Isfahan University of Medical Sciences · IRThomas Jefferson University · US

Funding

Mechanisms of GM-CSF effect in CNS autoimmune demyelinationR01AI124386 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2017 to 2021
$1.9M
The Role of GM-CSF in the Pathogenesis of Multiple SclerosisR01NS088729 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2014 to 2018
$1.7M
NIAID NIH HHS R01 AI124386NINDS NIH HHS R01 NS088729
6 · The paper itself

Abstract

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a multipotent cytokine that prompts the proliferation of bone marrow-derived macrophages and granulocytes. In addition to its effects as a growth factor, GM-CSF plays an important role in chronic inflammatory autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. Reports have identified monocytes as the primary target of GM-CSF; however, its effect on monocyte activation has been under-estimated. Here, using flow cytometry and ELISA we show that GM-CSF induces an inflammatory profile in human monocytes, which includes an upregulated expression of HLA-DR and CD86 molecules and increased production of TNF-α and IL-1β. Conversely, blockage of endogenous GM-CSF with antibody treatment not only inhibited the inflammatory profile of these cells, but also induced an immunomodulatory one, as shown by increased IL-10 production by monocytes. Further analysis with qPCR, flow cytometry and ELISA experiments revealed that GM-CSF blockage in monocytes stimulated production of the chemokine CXCL-11, which suppressed T cell proliferation. Blockade of CXCL-11 abrogated anti-GM-CSF treatment and induced inflammatory monocytes. Our findings show that anti-GM-CSF treatment induces modulatory monocytes that act in a CXCL-11-dependent manner, a mechanism that can be used in the development of novel approaches to treat chronic inflammatory autoimmune diseases.

Indexed as

B7-2 AntigenChemokine CXCL11Enzyme-Linked Immunosorbent AssayFlow CytometryGranulocyte-Macrophage Colony-Stimulating FactorHLA-DR AntigensHumansInterleukin-10Interleukin-1betaMonocytesPhenotypeReal-Time Polymerase Chain ReactionTumor Necrosis Factor-alphaB7-2 AntigenChemokine CXCL11Granulocyte-Macrophage Colony-Stimulating FactorHLA-DR AntigensInterleukin-10Interleukin-1betaTumor Necrosis Factor-alpha

Identifiers

PMID32005854
PMCPMC6994676
OpenAlexW3003654749

What OpenQuestion holds

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Registered trials

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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.