Evidence map›Paper›PMID 22529298›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Mast cell TLR2 signaling is crucial for effective killing of Francisella tularensis.

Annette R Rodriguez, Jieh-Juen Yu, M Neal Guentzel, Christopher S Navara, Karl E Klose, Thomas G Forsthuber, James P Chambers, Michael T Berton, Bernard P Arulanandam

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. The immune response toFrontiers in microbiology · 2025
    Review
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  13. Mast cell function: a new vision of an old cell.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014
    Review
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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

9 authors at 3 institutions in 1 country.

Annette R RodriguezSouth Texas Center for Emerging Infectious Diseases, University of Texas at San Antonio, San Antonio, TX 78249, USA.
Jieh-Juen Yu
M Neal Guentzel
Christopher S Navara
Karl E Klose
Thomas G Forsthuber
James P Chambers
Michael T Berton
Bernard P Arulanandam
Texas Center for Infectious Disease · USThe University of Texas at San Antonio · USThe University of Texas Health Science Center at San Antonio · US

Funding

UTSA RISE Research Training ProgramR25GM060655 · NIGMS · UNIVERSITY OF TEXAS SAN ANTONIO · PI BAREA-RODRIGUEZ, EDWIN J · 2000 to 2022
$21.6M
Tularemia: Pathogenesis and Host ResponseP01AI057986 · NIAID · UNIVERSITY OF TEXAS SAN ANTONIO · PI KLOSE, KARL E · 2005 to 2009
$6.1M
NIAID NIH HHS P01 AI057986NIGMS NIH HHS GM60655NIGMS NIH HHS R25 GM060655
6 · The paper itself

Abstract

TLR signaling is critical for early host defense against pathogens, but the contributions of mast cell TLR-mediated mechanisms and subsequent effector functions during pulmonary infection are largely unknown. We have previously demonstrated that mast cells, through the production of IL-4, effectively control Francisella tularensis replication. In this study, the highly human virulent strain of F. tularensis SCHU S4 and the live vaccine strain were used to investigate the contribution of mast cell/TLR regulation of Francisella. Mast cells required TLR2 for effective bacterial killing, regulation of the hydrolytic enzyme cathepsin L, and for coordination and trafficking of MHC class II and lysosomal-associated membrane protein 2. Infected TLR2(-/-) mast cells, in contrast to wild-type and TLR4(-/-) cells, lacked detectable IL-4 and displayed increased cell death with a 2-3 log increase of F. tularensis replication, but could be rescued with rIL-4 treatment. Importantly, MHC class II and lysosomal-associated membrane protein 2 localization with labeled F. tularensis in the lungs was greater in wild-type than in TLR2(-/-) mice. These results provide evidence for the important effector contribution of mast cells and TLR2-mediated signaling on early innate processes in the lung following pulmonary F. tularensis infection and provide additional insight into possible mechanisms by which intracellular pathogens modulate respiratory immune defenses.

Indexed as

AnimalsCell DeathFrancisella tularensisInterleukin-4Mast CellsMiceMice, Inbred C57BLMice, KnockoutProtein TransportSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4TularemiaInterleukin-4Tlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID22529298
PMCPMC3358431
OpenAlexW2146752396

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.