Evidence map›Paper›PMID 19064255›Full record

ArticleCell host & microbe2008

TLR-independent type I interferon induction in response to an extracellular bacterial pathogen via intracellular recognition of its DNA.

Marie Charrel-Dennis, Eicke Latz, Kristen A Halmen, Patrick Trieu-Cuot, Katherine A Fitzgerald, Dennis L Kasper, Douglas T Golenbock

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

83 citing papers in PubMed, 138 citations in OpenAlex.

  1. Trial
  2. Gut microbes · 2026
    Article
  3. Frontiers in immunology · 2025
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  4. Review
  5. Article
  6. Article
  7. Review
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  11. Article
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  14. Article
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  16. Article
  17. Cyclic GMP-AMP Synthase Is the Cytosolic Sensor ofJournal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  18. Review
  19. Article
  20. Review

23 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

7 authors at 3 institutions in 2 countries.

Marie Charrel-DennisDepartment of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Eicke Latz
Kristen A Halmen
Patrick Trieu-Cuot
Katherine A Fitzgerald
Dennis L Kasper
Douglas T Golenbock
University of Massachusetts Chan Medical School · USBrigham and Women's Hospital · USCentre National de la Recherche Scientifique · FR

Funding

INFECTIOUS DISEASE AND BASIC MICROBIOLOGICAL MECHANISMST32AI007061 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Marcia B Goldberg · 1985 to 2026
$12.1M
Gene Regulation in Innate ImmunityR37AI067497 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FITZGERALD, KATHERINE A. · 2015 to 2024
$4.6M
Group B. Streptococci and Toll-like ReceptorsR01AI052455 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GOLENBOCK, DOUGLAS T · 2002 to 2012
$4.2M
Regulation of Type I Interferon Gene Expression in the Innate Immune ResponseR01AI067497 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FITZGERALD, KATHERINE A. · 2006 to 2010
$2.0M
Regulation of Type I Interferon Gene Expression in the Innate Immune ResponseR56AI067497 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FITZGERALD, KATHERINE A. · 2012 to 2012
$415k
Group B. Streptococci and Toll-like ReceptorsR56AI052455 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GOLENBOCK, DOUGLAS T. · 2007 to 2007
$187k
NIAID NIH HHS 2AI052455NIAID NIH HHS AI067497NIAID NIH HHS R01 AI052455NIAID NIH HHS R01 AI067497NIAID NIH HHS R37 AI067497NIAID NIH HHS R56 AI052455NIAID NIH HHS R56 AI067497NIAID NIH HHS T32 AI007061
6 · The paper itself

Abstract

Type I interferon (IFN) is an important host defense cytokine against intracellular pathogens, mainly viruses. In assessing IFN production in response to group B streptococcus (GBS), we find that IFN-beta was produced by macrophages upon stimulation with both heat-killed and live GBS. Exposure of macrophages to heat-killed GBS activated a Toll-like receptor (TLR)-dependent pathway, whereas live GBS activated a TLR/NOD/RIG-like receptor (RLR)-independent pathway. This latter pathway required bacterial phagocytosis, proteolytic bacterial degradation, and phagolysosomal membrane destruction by GBS pore-forming toxins, leading to the release of bacterial DNA into the cytosol. GBS DNA in the cytosol induced IFN-beta production via a pathway dependent on the activation of the serine-threonine kinase TBK1 and phosphorylation of the transcription factor IRF3. Thus, activation of IFN-alpha/-beta production during infection with GBS, commonly considered an extracellular pathogen, appears to result from the interaction of GBS DNA with a putative intracellular DNA sensor or receptor.

Indexed as

AnimalsCells, CulturedDNA, BacterialInterferon Regulatory Factor-3Interferon Type IMacrophagesMiceMice, Inbred C57BLMice, KnockoutProtein Serine-Threonine KinasesStreptococcus agalactiaeToll-Like ReceptorsDNA, BacterialInterferon Regulatory Factor-3Interferon Type IIrf3 protein, mouseProtein Serine-Threonine KinasesTbk1 protein, mouseToll-Like Receptors

Identifiers

PMID19064255
PMCPMC3727391
OpenAlexW2052566477

What OpenQuestion holds

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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.