Evidence map›Paper›PMID 19720834›Full record

ArticleThe Journal of biological chemistry2009

Interferons direct an effective innate response to Legionella pneumophila infection.

Courtney R Plumlee, Carolyn Lee, Amer A Beg, Thomas Decker, Howard A Shuman, Christian Schindler

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.0field-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

54 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
  2. Article
  3. Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026
    Article
  4. Review
  5. Review
  6. Review
  7. Characterization ofFrontiers in cellular and infection microbiology · 2024
    Article
  8. Infection and immunity · 2023
    Article
  9. DNA-Dependent Interferon Induction and Lung Inflammation inJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023
    Article
  10. Knowledge to Predict Pathogens:Microorganisms · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. 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

6 authors at 3 institutions in 2 countries.

Courtney R PlumleeDepartment of Biological Sciences, Columbia University, New York, New York 10032, USA.
Carolyn Lee
Amer A Beg
Thomas Decker
Howard A Shuman
Christian Schindler
Columbia University · USMoffitt Cancer Center · USUniversity of Vienna · AT

Funding

Hormones: Molecular Mechanism of Action and FunctionsT32DK007328 · NIDDK · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI KOUSTENI, STAVROULA · 1986 to 2025
$7.8M
GENETICS OF MONOCYTE KILLING BY BACTERIAR01AI023549 · NIAID · UNIVERSITY OF CHICAGO · PI SHUMAN, HOWARD A · 1986 to 2013
$6.8M
IMMUNOLOGICAL DISEASE MECHANISMST32AI007525 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GHOSH, SANKAR · 1997 to 2006
$2.3M
IFN-Is at the interface of Innate and Adpative ImmunityR01AI058211 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SCHINDLER, CHRISTIAN W · 2004 to 2010
$2.0M
Mechanisms of co-stimulatory molecule expression in DCsR01AI059715 · NIAID · H. LEE MOFFITT CANCER CTR & RES INST · PI BEG, AMER AZIZ · 2005 to 2009
$1.7M
IL 3, IL 5, AND GM-CSF SIGNALING AND ASTHMAR01HL055413 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SCHINDLER, CHRISTIAN W · 1996 to 2004
$1.3M
Austrian Science Fund FWF P 20522NHLBI NIH HHS HL 55413NHLBI NIH HHS R01 HL055413NIAID NIH HHS 5T32 AI07525NIAID NIH HHS AI 058211NIAID NIH HHS AI 059715NIAID NIH HHS AI23549NIAID NIH HHS R01 AI023549NIAID NIH HHS R01 AI058211NIAID NIH HHS R01 AI059715NIAID NIH HHS T32 AI007525NIDDK NIH HHS 5T32 DK007328NIDDK NIH HHS T32 DK007328
6 · The paper itself

Abstract

Legionella pneumophila remains an important opportunistic pathogen of human macrophages. Its more limited ability to replicate in murine macrophages has been attributed to redundant innate sensor systems that detect and effectively respond to this infection. The current studies evaluate the role of one of these innate response systems, the type I interferon (IFN-I) autocrine loop. The ability of L. pneumophila to induce IFN-I expression was found to be dependent on IRF-3, but not NF-kappaB. Secreted IFN-Is then in turn suppress the intracellular replication of L. pneumophila. Surprisingly, this suppression is mediated by a pathway that is independent of Stat1, Stat2, Stat3, but correlates with the polarization of macrophages toward the M1 or classically activated phenotype.

Indexed as

Immunity, InnateAnimalsAutocrine CommunicationCells, CulturedInterferonsInterferon Type ILegionella pneumophilaLegionnaires' DiseaseMacrophage ActivationMacrophagesMiceNF-kappa BSTAT Transcription FactorsInterferonsInterferon Type INF-kappa BSTAT Transcription Factors

Identifiers

PMID19720834
PMCPMC2781560
OpenAlexW2081393349

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.