Evidence map›Paper›PMID 27549173›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Differential Production of Type I IFN Determines the Reciprocal Levels of IL-10 and Proinflammatory Cytokines Produced by C57BL/6 and BALB/c Macrophages.

Ashleigh Howes, Christina Taubert, Simon Blankley, Natasha Spink, Xuemei Wu, Christine M Graham, Jiawen Zhao, Margarida Saraiva, Paola Ricciardi-Castagnoli, Gregory J Bancroft and 1 more

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Loss of TRIM24 promotes IL-10 expression via CBP/p300-dependent IFNβ1 transcription during macrophage activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Biology and therapeutic potential of interleukin-10.The Journal of experimental medicine · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Type I interferons in tuberculosis: Foe and occasionally friend.The Journal of experimental medicine · 2018
    Review
  16. Article
  17. A Type I Interferon and IL-10 Induced byFrontiers in immunology · 2018
    Article
  18. Review
  19. Article
  20. Article
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

11 authors at 5 institutions in 5 countries.

Ashleigh HowesLaboratory of Immunoregulation and Infection, The Francis Crick Institute, Mill Hill Laboratory, London NW7 1AA, United Kingdom;
Christina TaubertLaboratory of Immunoregulation and Infection, The Francis Crick Institute, Mill Hill Laboratory, London NW7 1AA, United Kingdom;
Simon BlankleyLaboratory of Immunoregulation and Infection, The Francis Crick Institute, Mill Hill Laboratory, London NW7 1AA, United Kingdom;
Natasha SpinkLondon School of Hygiene and Tropical Medicine, London WC1E 7HT, United Kingdom;
Xuemei WuLaboratory of Immunoregulation and Infection, The Francis Crick Institute, Mill Hill Laboratory, London NW7 1AA, United Kingdom;
Christine M GrahamLaboratory of Immunoregulation and Infection, The Francis Crick Institute, Mill Hill Laboratory, London NW7 1AA, United Kingdom;
Jiawen ZhaoDepartment of Research and Innovation, Neo-Life Stem Cell Biotech Inc., Sichuan Umbilical Cord Blood Bank, Chengdu, Sichuan 610036, People's Republic of China;
Margarida SaraivaLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, 4710-057 Braga, Portugal; Life and Health Sciences Research Institute, Biomaterials, Biodegradables and Biomimetics, Portuguese Government Associate Laboratory, 4710-057 Braga/Guimarães, Portugal;
Paola Ricciardi-CastagnoliSingapore Immunology Network, Agency for Science, Technology and Research, Singapore 138632, Singapore; and.ORCID 0000-0002-4749-7187
Gregory J BancroftLondon School of Hygiene and Tropical Medicine, London WC1E 7HT, United Kingdom;ORCID 0000-0002-7243-679X
Anne O'GarraLaboratory of Immunoregulation and Infection, The Francis Crick Institute, Mill Hill Laboratory, London NW7 1AA, United Kingdom; Department of Medicine, National Heart and Lung Institute, Imperial College London, London SW3 6LY, United Kingdom Anne.OGarra@crick.ac.uk.ORCID 0000-0001-9845-6134
The Francis Crick Institute · GBUniversity of London · GBAgency for Science, Technology and Research · SGCell Technology (China) · CNUniversity of Minho · PT

Funding

Cancer Research UK FC001126Medical Research Council MC_U117565642Medical Research Council MR/J010723/1Wellcome Trust FC001126
6 · The paper itself

Abstract

Pattern recognition receptors detect microbial products and induce cytokines, which shape the immunological response. IL-12, TNF-α, and IL-1β are proinflammatory cytokines, which are essential for resistance against infection, but when produced at high levels they may contribute to immunopathology. In contrast, IL-10 is an immunosuppressive cytokine, which dampens proinflammatory responses, but it can also lead to defective pathogen clearance. The regulation of these cytokines is therefore central to the generation of an effective but balanced immune response. In this study, we show that macrophages derived from C57BL/6 mice produce low levels of IL-12, TNF-α, and IL-1β, but high levels of IL-10, in response to TLR4 and TLR2 ligands LPS and Pam3CSK4, as well as Burkholderia pseudomallei, a Gram-negative bacterium that activates TLR2/4. In contrast, macrophages derived from BALB/c mice show a reciprocal pattern of cytokine production. Differential production of IL-10 in B. pseudomallei and LPS-stimulated C57BL/6 and BALB/c macrophages was due to a type I IFN and ERK1/2-dependent, but IL-27-independent, mechanism. Enhanced type I IFN expression in LPS-stimulated C57BL/6 macrophages was accompanied by increased STAT1 and IFN regulatory factor 3 activation. Furthermore, type I IFN contributed to differential IL-1β and IL-12 production in B. pseudomallei and LPS-stimulated C57BL/6 and BALB/c macrophages via both IL-10-dependent and -independent mechanisms. These findings highlight key pathways responsible for the regulation of pro- and anti-inflammatory cytokines in macrophages and reveal how they may differ according to the genetic background of the host.

Indexed as

AnimalsBurkholderia pseudomalleiCytokinesInflammationInterferon Type IInterleukin-10LipopolysaccharidesMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutCytokinesInterferon Type IInterleukin-10Lipopolysaccharides

Identifiers

PMID27549173
PMCPMC5026030
OpenAlexW2515528675

What OpenQuestion holds

Textmetadata
LicenceTDM
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.