Evidence map›Paper›PMID 27670945›Full record

ArticleInnate immunity2016

Regulation of the IL-10-driven macrophage phenotype under incoherent stimuli.

Yishan Chuang, Michelle E Hung, Brianne K Cangelose, Joshua N Leonard

Open access · bronzeAbstract read
In one paragraph

Article in Innate immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

52 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  8. Review
  9. Inhibition of hedgehog signaling ameliorates severity of chronic pancreatitis in experimental mouse models.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  10. Review
  11. Article
  12. Macrophage fate: to kill or not to kill?Infection and immunity · 2024
    Review
  13. Review
  14. Article
  15. Osteoarthritis and cartilage open · 2024
    Article
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

Yishan Chuang1 Department of Chemical and Biological Engineering, Northwestern University, USA.
Michelle E Hung2 Interdisciplinary Biological Sciences Program, Northwestern University, USA.
Brianne K Cangelose1 Department of Chemical and Biological Engineering, Northwestern University, USA.
Joshua N Leonard1 Department of Chemical and Biological Engineering, Northwestern University, USA.
Northwestern University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
TRANS-NETWORK PROJECTSU54CA143869 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MARKO, JOHN F · 2009 to 2013
$12.8M
Spatio-Temporal Organization of Chromatin and Information Transfer in CancerU54CA193419 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BACKMAN, VADIM · 2015 to 2020
$10.4M
NCI NIH HHS P30 CA060553NCI NIH HHS U54 CA143869NCI NIH HHS U54 CA193419
6 · The paper itself

Abstract

Macrophages are ubiquitous innate immune cells that play a central role in health and disease by adopting distinct phenotypes, which are broadly divided into classical inflammatory responses and alternative responses that promote immune suppression and wound healing. Although macrophages are attractive therapeutic targets, incomplete understanding of this functional choice limits clinical manipulation. While individual stimuli, pathways, and genes involved in macrophage functional responses have been identified, how macrophages evaluate complex in vivo milieus comprising multiple divergent stimuli remains poorly understood. Here, we used combinations of "incoherent" stimuli-those that individually promote distinct macrophage phenotypes-to elucidate how the immunosuppressive, IL-10-driven macrophage phenotype is induced, maintained, and modulated under such combinatorial stimuli. The IL-10-induced immunosuppressive phenotype was largely insensitive to co-administered IL-12, which has been reported to modulate macrophage phenotype, but maintaining the immunosuppressive phenotype required sustained exposure to IL-10. Our data implicate the intracellular protein, BCL3, as a key mediator of the IL-10-driven phenotype. Notably, co-administration of IFN-γ disrupted an IL-10-mediated positive feedback loop that may reinforce the immunosuppressive phenotype. This novel combinatorial perturbation approach thus generated new insights into macrophage decision making and local immune network function.

Indexed as

Cell DifferentiationAnimalsB-Cell Lymphoma 3 ProteinFeedback, PhysiologicalImmunity, InnateImmunosuppression TherapyInterferon-gammaInterleukin-10Interleukin-12MacrophagesMaleMiceMice, Inbred C57BLPhenotypeProto-Oncogene ProteinsRAW 264.7 CellsB-Cell Lymphoma 3 ProteinBcl3 protein, mouseInterferon-gammaInterleukin-10Interleukin-12Proto-Oncogene ProteinsTranscription FactorsInterleukin-10 (IL-10)macrophage polarizationmacrophagestumor-associated macrophages (TAM)

Identifiers

PMID27670945
PMCPMC5292318
OpenAlexW2523772128

What OpenQuestion holds

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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.