Evidence map›Paper›PMID 26020782›Full record

ArticlePLoS pathogens2015

Ly6C- Monocytes Regulate Parasite-Induced Liver Inflammation by Inducing the Differentiation of Pathogenic Ly6C+ Monocytes into Macrophages.

Yannick Morias, Chloé Abels, Damya Laoui, Eva Van Overmeire, Martin Guilliams, Elio Schouppe, Frank Tacke, Carlie J deVries, Patrick De Baetselier, Alain Beschin

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  7. Hepatic Ly6CJournal of clinical medicine · 2022
    Article
  8. Pathogens (Basel, Switzerland) · 2022
    Article
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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

10 authors at 5 institutions in 3 countries.

Yannick MoriasMyeloid Cell Immunology Laboratory, Vlaams Instituut voor Biotechnologie (VIB), Brussels, Belgium; Cellular and Molecular Immunology Unit, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
Chloé AbelsMyeloid Cell Immunology Laboratory, Vlaams Instituut voor Biotechnologie (VIB), Brussels, Belgium; Cellular and Molecular Immunology Unit, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
Damya LaouiMyeloid Cell Immunology Laboratory, Vlaams Instituut voor Biotechnologie (VIB), Brussels, Belgium; Cellular and Molecular Immunology Unit, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
Eva Van OvermeireMyeloid Cell Immunology Laboratory, Vlaams Instituut voor Biotechnologie (VIB), Brussels, Belgium; Cellular and Molecular Immunology Unit, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
Martin GuilliamsInflammation Research Center, Vlaams Instituut voor Biotechnologie (VIB), Ghent, Belgium; Laboratory of Immunoregulation and Mucosal Immunology, University Gent, Gent, Belgium.
Elio SchouppeMyeloid Cell Immunology Laboratory, Vlaams Instituut voor Biotechnologie (VIB), Brussels, Belgium; Cellular and Molecular Immunology Unit, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
Frank TackeDepartment of Medicine III, Rheinisch-Westfaelische Technische Hochschule (RWTH) University Hospital Aachen, Aachen, Germany.
Carlie J deVriesDepartment of Medical Biochemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Patrick De BaetselierMyeloid Cell Immunology Laboratory, Vlaams Instituut voor Biotechnologie (VIB), Brussels, Belgium; Cellular and Molecular Immunology Unit, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
Alain BeschinMyeloid Cell Immunology Laboratory, Vlaams Instituut voor Biotechnologie (VIB), Brussels, Belgium; Cellular and Molecular Immunology Unit, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
Vrije Universiteit Brussel · BEAcademic Medical Center · NLGhent University · BEUniversitätsklinikum Aachen · DEVlaams Instituut voor Biotechnologie · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocytes consist of two well-defined subsets, the Ly6C+ and Ly6C- monocytes. Both CD11b+ myeloid cells populations have been proposed to infiltrate tissues during inflammation. While infiltration of Ly6C+ monocytes is an established pathogenic factor during hepatic inflammation, the role of Ly6C- monocytes remains elusive. Mice suffering experimental African trypanosome infection die from systemic inflammatory response syndrome (SIRS) that is initiated by phagocytosis of parasites by liver myeloid cells and culminates in apoptosis/necrosis of liver myeloid and parenchymal cells that reduces host survival. C57BL/6 mice are considered as trypanotolerant to Trypanosoma congolense infection. We have reported that in these animals, IL-10, produced among others by myeloid cells, limits the liver damage caused by pathogenic TNF-producing Ly6C+ monocytes, ensuring prolonged survival. Here, the heterogeneity and dynamics of liver myeloid cells in T. congolense-infected C57/BL6 mice was further dissected. Moreover, the contribution of Ly6C- monocytes to trypanotolerance was investigated. By using FACS analysis and adoptive transfer experiments, we found that the accumulation of Ly6C- monocytes and macrophages in the liver of infected mice coincided with a drop in the pool of Ly6C+ monocytes. Pathogenic TNF mainly originated from Ly6C+ monocytes while Ly6C- monocytes and macrophages were major and equipotent sources of IL-10 within myeloid cells. Moreover, Nr4a1 (Nur77) transcription factor-dependent Ly6C- monocytes exhibited IL-10-dependent and cell contact-dependent regulatory properties contributing to trypanotolerance by suppressing the production of TNF by Ly6C+ monocytes and by promoting the differentiation of the latter cells into macrophages. Thus, Ly6C- monocytes can dampen liver damage caused by an extensive Ly6C+ monocyte-associated inflammatory immune response in T. congolense trypanotolerant animals. In a more general context, Ly6C- or Ly6C+ monocyte targeting may represent a therapeutic approach in liver pathogenicity induced by chronic infection.

Indexed as

Cell DifferentiationAnimalsAntigens, LyApoptosisBlotting, WesternCell ProliferationFemaleFlow CytometryImmunoenzyme TechniquesInflammationInterleukin-10Liver DiseasesMacrophagesMiceMice, Inbred C57BLMonocytesAntigens, LyInterleukin-10RNA, Messenger

Identifiers

PMID26020782
PMCPMC4447383
OpenAlexW2157587971

What OpenQuestion holds

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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.