Evidence map›Paper›PMID 17397264›Full record

ArticlePLoS pathogens2007

Bacterial ligands generated in a phagosome are targets of the cytosolic innate immune system.

Anat A Herskovits, Victoria Auerbuch, Daniel A Portnoy

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 161 citations in OpenAlex.

  1. Trial
  2. Wound-Healing Potential of Engineered Lysin GRC-ML07 inAntibiotics (Basel, Switzerland) · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Pattern Recognition by NOD-Like Receptors.Advances in experimental medicine and biology · 2025
    Review
  7. Minimalist TetrazineJournal of the American Chemical Society · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. The Journal of biological chemistry · 2020
    Article
  17. Article
  18. Article
  19. Review
  20. Cas9eLife · 2019
    Article

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

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

3 authors at 1 institution in 1 country.

Anat A HerskovitsDepartment of Molecular and Cell Biology, University of California, Berkeley, California, United States of America.
Victoria Auerbuch
Daniel A Portnoy
University of California, Berkeley · US

Funding

The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI STANLEY, SARAH A · 2004 to 2025
$45.5M
Listeria Hemolysis and Escape From a VacuoleR01AI027655 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI DANIEL A PORTNOY · 1993 to 2026
$10.1M
NIAID NIH HHS P01 AI063302NIAID NIH HHS R01 AI027655
6 · The paper itself

Abstract

Macrophages are permissive hosts to intracellular pathogens, but upon activation become microbiocidal effectors of innate and cell-mediated immunity. How the fate of internalized microorganisms is monitored by macrophages, and how that information is integrated to stimulate specific immune responses is not understood. Activation of macrophages with interferon (IFN)-gamma leads to rapid killing and degradation of Listeria monocytogenes in a phagosome, thus preventing escape of bacteria to the cytosol. Here, we show that activated macrophages induce a specific gene expression program to L. monocytogenes degraded in the phago-lysosome. In addition to activation of Toll-like receptor (TLR) signaling pathways, degraded bacteria also activated a TLR-independent transcriptional response that was similar to the response induced by cytosolic L. monocytogenes. More specifically, degraded bacteria induced a TLR-independent IFN-beta response that was previously shown to be specific to cytosolic bacteria and not to intact bacteria localized to the phagosome. This response required the generation of bacterial ligands in the phago-lysosome and was largely dependent on nucleotide-binding oligomerization domain 2 (NOD2), a cytosolic receptor known to respond to bacterial peptidoglycan fragments. The NOD2-dependent response to degraded bacteria required the phagosomal membrane potential and the activity of lysosomal proteases. The NOD2-dependent IFN-beta production resulted from synergism with other cytosolic microbial sensors. This study supports the hypothesis that in activated macrophages, cytosolic innate immune receptors are activated by bacterial ligands generated in the phagosome and transported to the cytosol.

Indexed as

AnimalsBacterial ProteinsCells, CulturedCytosolGene Expression Regulation, BacterialImmunity, InnateInterferon-betaLigandsListeria monocytogenesListeriosisMacrophage ActivationMacrophagesMembrane PotentialsMiceMice, Inbred C57BLNod2 Signaling Adaptor ProteinBacterial ProteinsInterferon-betaLigandsNod2 protein, mouseNod2 Signaling Adaptor ProteinToll-Like Receptors

Identifiers

PMID17397264
PMCPMC1839167
OpenAlexW1980223460

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.