Evidence map›Paper›PMID 23475311›Full record

ArticleThe Journal of infectious diseases2013

Mycobacterium tuberculosis exploits human interferon γ to stimulate macrophage extracellular trap formation and necrosis.

Ka-Wing Wong, Williams R Jacobs

Open access · hybridAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
5.6field-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

92 citing papers in PubMed, 140 citations in OpenAlex.

  1. Review
  2. Article
  3. Macrophage Extracellular Traps in Immunity and Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Macrophage extracellular traps are induced by Mycoplasma bovis in bovine macrophages through NADPH oxidase/ROS-dependent manner and their antibacterial efficacy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  16. Review
  17. Emerging insights into macrophage extracellular traps in bacterial infections.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
  18. Review
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Ka-Wing WongDepartment of Microbiology and Immunology, Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Williams R Jacobs
Albert Einstein College of Medicine · USHoward Hughes Medical Institute · US

Funding

Immunology/Pathology CoreP30AI051519 · NIAID · YESHIVA UNIVERSITY · PI GOLDSTEIN, HARRIS · 2003 to 2013
$18.6M
"The Tuberculous Granuloma"P01AI063537 · NIAID · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI CHAN, JOHN R. · 2005 to 2015
$15.7M
MOLECULAR GENETIC ANALYSIS OF MYCOBACTERIUM TUBERCULOSISR01AI026170 · NIAID · YESHIVA UNIVERSITY · PI JACOBS, WILLIAM ROBERT · 1989 to 2022
$7.1M
NIAID NIH HHS AI0-51519NIAID NIH HHS P01 AI063537NIAID NIH HHS P30 AI051519NIAID NIH HHS R01 AI026170NIAID NIH HHS R01 AI26170
6 · The paper itself

Abstract

Human neutrophils form extracellular traps during M. tuberculosis infection, but a similar phenomenon has not been reported in human macrophages. Here we demonstrate that M. tuberculosis induces release of extracellular traps from human macrophages. This process is regulated by elastase activity, previously shown to regulate formation of extracellular traps by neutrophils. Interestingly, formation of extracellular traps by macrophages during M. tuberculosis infection is inducible by interferon γ (IFN-γ). These traps are mainly produced by heavily infected macrophages. Accordingly, IFN-γ is found to stimulate M. tuberculosis aggregation in macrophages. Both IFN-γ-inducible events, extracellular trap formation and mycobacterial aggregation, require the ESX-1 secretion system. In addition, IFN-γ is found to enhance ESX-1-mediated macrophage necrosis. In the absence of ESX-1, IFN-γ does not restore any extracellular trap formation, mycobacterial aggregation, or macrophage necrosis. Thus, initial characterization of macrophage extracellular trap formation due to M. tuberculosis infection led to the uncovering of a novel role for IFN-γ in amplifying multiple effects of the mycobacterial ESX-1.

Indexed as

Homeodomain ProteinsHumansInterferon-gammaMacrophagesMycobacterium tuberculosisNecrosisTuberculosisESX1 protein, humanHomeodomain ProteinsInterferon-gammaESX-1extracellular trapshuman macrophagesinterferon-γM. tuberculosisnecrosis

Identifiers

PMID23475311
PMCPMC3666134
OpenAlexW2111236188

What OpenQuestion holds

Textmetadata
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.