Evidence map›Paper›PMID 17785474›Full record

ArticleInfection and immunity2007

Toll-like receptor 2 controls the gamma interferon response to Francisella tularensis by mouse liver lymphocytes.

Kee-Jong Hong, Jason R Wickstrum, Hung-Wen Yeh, Michael J Parmely

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

24 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
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  4. Innate Immune Recognition: Implications for the Interaction ofFrontiers in cellular and infection microbiology · 2017
    Review
  5. Mitogen-activated protein kinases (MAPKs) are modulated during Francisella tularensis infection, but inhibition of extracellular-signal-regulated kinases (ERKs) is of limited therapeutic benefit.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016
    Article
  6. Review
  7. Review
  8. Article
  9. Article
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  13. IL-23 in infections, inflammation, autoimmunity and cancer: possible role in HIV-1 and AIDS.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012
    Review
  14. Article
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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

4 authors at 1 institution in 1 country.

Kee-Jong HongDepartment of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160, USA.
Jason R Wickstrum
Hung-Wen Yeh
Michael J Parmely
University of Kansas Medical Center · US

Funding

Innate Immunity to Francisella tularensisR21AI062939 · NIAID · UNIVERSITY OF KANSAS MEDICAL CENTER · PI PARMELY, MICHAEL J · 2005 to 2006
$400k
RESOURCES FOR PROTEIN CRYSTALLOGRAPHYP41RR001644 · NCRR · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI XUONG, NGUYEN-HUU H · 1985 to 1995
–
NCRR NIH HHS P20 RR0164443NIAID NIH HHS R21 AI062939
6 · The paper itself

Abstract

The production of gamma interferon (IFN-gamma) is a key step in the protective innate immune response to Francisella tularensis. Natural killer cells and T cells in the liver are important sources of this cytokine during primary F. tularensis infections, and interleukin-12 (IL-12) appears to be an essential coactivating cytokine for hepatic IFN-gamma expression. The present study was undertaken to determine whether or not macrophages (Mphi) or dendritic cells (DC) provide coactivating signals for the liver IFN-gamma response in vitro, whether IL-12 mediates these effects, and whether Toll-like receptor (TLR) signaling is essential to induce this costimulatory activity. Both bone marrow-derived Mphi and DC significantly augmented the IFN-gamma response of F. tularensis-challenged liver lymphocytes in vitro. While both cell types produced IL-12p40 in response to F. tularensis challenge, only DC secreted large quantities of IL-12p70. DC from both IL-12p35-deficient and TLR2-deficient mice failed to produce IL-12p70 and did not costimulate liver lymphocytes for IFN-gamma production in response to viable F. tularensis organisms. Conversely, liver lymphocytes from TLR2-deficient mice cocultured with wild-type accessory cells produced IFN-gamma at levels comparable to those for wild-type hepatic lymphocytes. These findings indicate that TLR2 controls hepatic lymphocyte IFN-gamma responses to F. tularensis by regulating DC IL-12 production. While Mphi also coinduced hepatic IFN-gamma production in response to F. tularensis, they did so in a fashion less dependent on TLR2.

Indexed as

AnimalsCells, CulturedCoculture TechniquesDendritic CellsFemaleFrancisella tularensisInterferon-gammaInterleukin-12Interleukin-12 Subunit p35Interleukin-12 Subunit p40LiverMacrophagesMiceMice, Inbred C57BLMice, KnockoutT-LymphocytesInterferon-gammaInterleukin-12Interleukin-12 Subunit p35Interleukin-12 Subunit p40Toll-Like Receptor 2

Identifiers

PMID17785474
PMCPMC2168295
OpenAlexW2112791648

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.