Evidence map›Paper›PMID 21790939›Full record

ArticleCellular microbiology2011

Dissection of a type I interferon pathway in controlling bacterial intracellular infection in mice.

Juliane Lippmann, Holger C Müller, Jan Naujoks, Christoph Tabeling, Sunny Shin, Martin Witzenrath, Katharina Hellwig, Carsten J Kirschning, Gregory A Taylor, Winfried Barchet and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cellular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Diverse infection models demonstrate robust resistance ofbioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Infection and immunity · 2023
    Article
  11. TheProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. CLEC12A Binds toInternational journal of molecular sciences · 2023
    Article
  13. Review
  14. Article
  15. Review
  16. Knowledge to Predict Pathogens:Microorganisms · 2022
    Review
  17. Article
  18. Review
  19. Review
  20. Review
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

14 authors at 4 institutions in 2 countries.

Juliane LippmannDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany.
Holger C Müller
Jan Naujoks
Christoph Tabeling
Sunny Shin
Martin Witzenrath
Katharina Hellwig
Carsten J Kirschning
Gregory A Taylor
Winfried Barchet
Stefan Bauer
Norbert Suttorp
Craig R Roy
Bastian Opitz
Charité - Universitätsmedizin Berlin · DEYale University · USGeriatric Research Education and Clinical Center · USUniversity of Duisburg-Essen · DE

Funding

EVASION OF ANTIGEN PRESENTATION BY VACUOLAR PATHOGENSR01AI048770 · NIAID · YALE UNIVERSITY · PI ROY, CRAIG R. · 2001 to 2015
$5.8M
Regulation of IFN-g-induced Innate Immunity by LRG-47R01AI057831 · NIAID · DUKE UNIVERSITY · PI TAYLOR, GREGORY A · 2004 to 2013
$3.1M
NIAID NIH HHS AI57831NIAID NIH HHS R01 AI048770NIAID NIH HHS R01 AI057831
6 · The paper itself

Abstract

Defence mechanisms against intracellular bacterial pathogens are incompletely understood. Our study characterizes a type I IFN-dependent cell-autonomous defence pathway directed against Legionella pneumophila, an intracellular model organism and frequent cause of pneumonia. We show that macrophages infected with L. pneumophila produced IFNβ in a STING- and IRF3- dependent manner. Paracrine type I IFNs stimulated upregulation of IFN-stimulated genes and a cell-autonomous defence pathway acting on replicating and non-replicating Legionella within their specialized vacuole. Our infection experiments in mice lacking receptors for type I and/or II IFNs show that type I IFNs contribute to expression of IFN-stimulated genes and to bacterial clearance as well as resistance in L. pneumophila pneumonia in addition to type II IFN. Overall, our study shows that paracrine type I IFNs mediate defence against L. pneumophila, and demonstrates a protective role of type I IFNs in in vivo infections with intracellular bacteria.

Indexed as

Signal TransductionAnimalsDisease Models, AnimalGene Expression ProfilingInterferon Regulatory Factor-3Interferon Type ILegionella pneumophilaLegionnaires' DiseaseMacrophagesMembrane ProteinsMiceSTING ProteinVacuolesInterferon Regulatory Factor-3Interferon Type IIrf3 protein, mouseMembrane ProteinsSting1 protein, mouseSTING Protein

Identifiers

PMID21790939
PMCPMC3196383
OpenAlexW1544733216

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.