Evidence map›Paper›PMID 15322028›Full record

ArticleInfection and immunity2004

Identification of Mycobacterium tuberculosis counterimmune (cim) mutants in immunodeficient mice by differential screening.

Katherine B Hisert, Meghan A Kirksey, James E Gomez, Alexandra O Sousa, Jeffery S Cox, William R Jacobs, Carl F Nathan, John D McKinney

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-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

21 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Howard A. Young's 4 Decades in Science: More Than Just Experiments.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Metabolic Perspectives on Persistence.Microbiology spectrum · 2017
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Mycobacterium tuberculosis persistence mutants identified by screening in isoniazid-treated mice.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  15. Review
  16. Expression profiling in granulomatous lung disease.Proceedings of the American Thoracic Society · 2007
    Review
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Katherine B HisertLaboratory of Infection Biology, The Rockefeller University, 1230 York Ave., New York, NY 10021, USA.
Meghan A Kirksey
James E Gomez
Alexandra O Sousa
Jeffery S Cox
William R Jacobs
Carl F Nathan
John D McKinney
Rockefeller University · USAlbert Einstein College of Medicine · USCornell University · USUniversity of California, San Francisco · US

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Molecular-genetic analysis of TB persistence and latencyR01AI051702 · NIAID · ROCKEFELLER UNIVERSITY · PI MCKINNEY, JOHN D. · 2002 to 2006
$1.7M
NIAID NIH HHS AI051702NIAID NIH HHS R01 AI051702NIGMS NIH HHS GM07739NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Tuberculosis (TB) is characterized by lifetime persistence of Mycobacterium tuberculosis. Despite the induction of a vigorous host immune response that curtails disease progression in the majority of cases, the organism is not eliminated. Subsequent immunosuppression can lead to reactivation after a prolonged period of clinical latency. Thus, while it is clear that protective immune mechanisms are engaged during M. tuberculosis infection, it also appears that the pathogen has evolved effective countermechanisms. Genetic studies with animal infection models and with patients have revealed a key role for the cytokine gamma interferon (IFN-gamma) in resistance to TB. IFN-gamma activates a large number of antimicrobial pathways. Three of these IFN-gamma-dependent mechanisms have been implicated in defense against M. tuberculosis: inducible nitric oxide synthase (iNOS), phagosome oxidase (phox), and the phagosome-associated GTPase LRG-47. In order to identify bacterial genes that provide protection against specific host immune pathways, we have developed the strategy of differential signature-tagged transposon mutagenesis. Using this approach we have identified three M. tuberculosis genes that are essential for progressive M. tuberculosis growth and rapid lethality in iNOS-deficient mice but not in IFN-gamma-deficient mice. We propose that these genes are involved in pathways that allow M. tuberculosis to counter IFN-gamma-dependent immune mechanisms other than iNOS.

Indexed as

MutationAnimalsBacterial ProteinsDNA Transposable ElementsFemaleHumansInterferon-gammaLungMaleMiceMice, Inbred C57BLMutagenesisMycobacterium tuberculosisNitric Oxide SynthaseNitric Oxide Synthase Type IITuberculosis, PulmonaryBacterial ProteinsDNA Transposable ElementsInterferon-gammaNitric Oxide SynthaseNitric Oxide Synthase Type IINOS2 protein, humanNos2 protein, mouse

Identifiers

PMID15322028
PMCPMC517420
OpenAlexW1979443300

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.