Evidence map›Paper›PMID 26482950›Full record

ArticleCell research2015

Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis.

Claire Lastrucci, Alan Bénard, Luciana Balboa, Karine Pingris, Shanti Souriant, Renaud Poincloux, Talal Al Saati, Voahangy Rasolofo, Pablo González-Montaner, Sandra Inwentarz and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 138 citations in OpenAlex.

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23 more citing papers are in PubMed but not listed here.

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

18 authors at 8 institutions in 4 countries.

Claire LastrucciCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Alan BénardCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Luciana BalboaInmunologia de Enfermedades Respiratorias, Instituto de Medicina Experimental (IMEX)-CONICET, Academia Nacional de Medicina, Pacheco de Melo 3081, 1425, Buenos Aires, Argentina.
Karine PingrisCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Shanti SouriantCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Renaud PoinclouxCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Talal Al SaatiINSERM/UPS-US006/CREFRE, Service d'Histopathologie, CHU Purpan, 31024, Toulouse, France.
Voahangy RasolofoMycobacteria Unit, Pasteur Institute in Antananarivo, Antananarivo, Madagascar.
Pablo González-MontanerInstituto Prof. Dr. Raúl Vaccarezza, Hospital de Infecciosas Dr. F.J. Muñiz, Buenos Aires, Argentina.
Sandra InwentarzInstituto Prof. Dr. Raúl Vaccarezza, Hospital de Infecciosas Dr. F.J. Muñiz, Buenos Aires, Argentina.
Eduardo Jose MorañaInstituto Prof. Dr. Raúl Vaccarezza, Hospital de Infecciosas Dr. F.J. Muñiz, Buenos Aires, Argentina.
Ivanela KondovaDepartment of Parasitology, Biomedical Primate Research Centre, Rijswijk, the Netherlands.
Frank A W VerreckDepartment of Parasitology, Biomedical Primate Research Centre, Rijswijk, the Netherlands.
Maria del Carmen SasiainInmunologia de Enfermedades Respiratorias, Instituto de Medicina Experimental (IMEX)-CONICET, Academia Nacional de Medicina, Pacheco de Melo 3081, 1425, Buenos Aires, Argentina.
Olivier NeyrollesCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Isabelle Maridonneau-PariniCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Geanncarlo Lugo-VillarinoCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Céline CougouleCNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Département of Tuberculosis and Infection Biology, Toulouse, France.
Centre National de la Recherche Scientifique · FRHospital Muñiz · ARUniversité Fédérale de Toulouse Midi-Pyrénées · FRUniversité Toulouse III - Paul Sabatier · FRAcademia Nacional de Medicina · ARBiomedical Primate Research Centre · NLInstitut de Pharmacologie et de Biologie Structurale · FRInstitut Pasteur de Madagascar · MG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human CD14(+) monocyte compartment is composed by two subsets based on CD16 expression. We previously reported that this compartment is perturbed in tuberculosis (TB) patients, as reflected by the expansion of CD16(+) monocytes along with disease severity. Whether this unbalance is beneficial or detrimental to host defense remains to be elucidated. Here in the context of active TB, we demonstrate that human monocytes are predisposed to differentiate towards an anti-inflammatory (M2-like) macrophage activation program characterized by the CD16(+)CD163(+)MerTK(+)pSTAT3(+) phenotype and functional properties such as enhanced protease-dependent motility, pathogen permissivity and immunomodulation. This process is dependent on STAT3 activation, and loss-of-function experiments point towards a detrimental role in host defense against TB. Importantly, we provide a critical correlation between the abundance of the CD16(+)CD163(+)MerTK(+)pSTAT3(+) cells and the progression of the disease either at the local level in a non-human primate tuberculous granuloma context, or at the systemic level through the detection of the soluble form of CD163 in human sera. Collectively, this study argues for the pathogenic role of the CD16(+)CD163(+)MerTK(+)pSTAT3(+) monocyte-to-macrophage differentiation program and its potential as a target for TB therapy, and promotes the detection of circulating CD163 as a potential biomarker for disease progression and monitoring of treatment efficacy.

Indexed as

ImmunomodulationHumansInterleukin-10MonocytesReceptors, IgGSTAT3 Transcription FactorTuberculosisIL10 protein, humanInterleukin-10Receptors, IgGSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID26482950
PMCPMC4670988
OpenAlexW1810065880

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.