Evidence map›Paper›PMID 23864618›Full record

ArticleJournal of virology2013

Human cytomegalovirus interleukin-10 polarizes monocytes toward a deactivated M2c phenotype to repress host immune responses.

Selmir Avdic, John Z Cao, Brian P McSharry, Leighton E Clancy, Rebecca Brown, Megan Steain, David J Gottlieb, Allison Abendroth, Barry Slobedman

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 80 citations in OpenAlex.

  1. Detection of Human CytomegalovirusThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2026
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  18. Human Cytomegalovirus Interleukin 10 Homologs: Facing the Immune System.Frontiers in cellular and infection microbiology · 2020
    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

9 authors at 2 institutions in 1 country.

Selmir AvdicCentre for Virus Research, Westmead Millennium Institute, Westmead, New South Wales, Australia.
John Z Cao
Brian P McSharry
Leighton E Clancy
Rebecca Brown
Megan Steain
David J Gottlieb
Allison Abendroth
Barry Slobedman
University of Sydney · AUWestmead Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several human cytomegalovirus (HCMV) genes encode products that modulate cellular functions in a manner likely to enhance viral pathogenesis. This includes UL111A, which encodes homologs of human interleukin-10 (hIL-10). Depending upon signals received, monocytes and macrophages become polarized to either classically activated (M1 proinflammatory) or alternatively activated (M2 anti-inflammatory) subsets. Skewing of polarization toward an M2 subset may benefit the virus by limiting the proinflammatory responses to infection, and so we determined whether HCMV-encoded viral IL-10 influenced monocyte polarization. Recombinant viral IL-10 protein polarized CD14(+) monocytes toward an anti-inflammatory M2 subset with an M2c phenotype, as demonstrated by high expression of CD163 and CD14 and suppression of major histocompatibility complex (MHC) class II. Significantly, in the context of productive HCMV infection, viral IL-10 produced by infected cells polarized uninfected monocytes toward an M2c phenotype. We also assessed the impact of viral IL-10 on heme oxygenase 1 (HO-1), which is an enzyme linked with suppression of inflammatory responses. Polarization of monocytes by viral IL-10 resulted in upregulation of HO-1, and inhibition of HO-1 function resulted in a loss of capacity of viral IL-10 to suppress tumor necrosis factor alpha (TNF-α) and IL-1β, implicating HO-1 in viral IL-10-induced suppression of proinflammatory cytokines by M2c monocytes. In addition, a functional consequence of monocytes polarized with viral IL-10 was a decreased capacity to activate CD4(+) T cells. This study identifies a novel role for viral IL-10 in driving M2c polarization, which may limit virus clearance by restricting proinflammatory and CD4(+) T cell responses at sites of infection.

Indexed as

Host-Pathogen InteractionsImmune EvasionAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCytomegalovirusHeme Oxygenase-1Histocompatibility Antigens Class IIHumansInterleukin-10Lipopolysaccharide ReceptorsMonocytesReceptors, Cell SurfaceViral ProteinsVirulence FactorsAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenHeme Oxygenase-1Histocompatibility Antigens Class IIInterleukin-10Lipopolysaccharide ReceptorsReceptors, Cell SurfaceViral ProteinsVirulence Factors

Identifiers

PMID23864618
PMCPMC3754025
OpenAlexW2114692134

What OpenQuestion holds

Textmetadata
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.