Evidence map›Paper›PMID 24598055›Full record

ArticleJournal of leukocyte biology2014

TLR ligands up-regulate Trex1 expression in murine conventional dendritic cells through type I Interferon and NF-κB-dependent signaling pathways.

Jun Xu, Philip W Zoltick, Ana M Gamero, Stefania Gallucci

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Autoinflammatory syndromes of STING and TREX1 dysfunction.The Journal of clinical investigation · 2026
    Review
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  12. The Role of Nucleic Acid Sensing in Controlling Microbial and Autoimmune Disorders.International review of cell and molecular biology · 2019
    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

4 authors at 2 institutions in 1 country.

Jun XuLaboratory of Dendritic Cell Biology, Department of Microbiology and Immunology, and.
Philip W ZoltickDepartment of Surgery, The Children's Center for Fetal Research, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Ana M GameroDepartment of Biochemistry, Temple University, School of Medicine, Philadelphia, Pennsylvania, USA; and.
Stefania GallucciLaboratory of Dendritic Cell Biology, Department of Microbiology and Immunology, and gallucci@temple.edu.
Children's Hospital of Philadelphia · USTemple University · US

Funding

Regulation of Type I IFNs in Tolerance and AutoimmunityR01AI076423 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI GALLUCCI, STEFANIA · 2009 to 2013
$1.7M
NIAID NIH HHS R01 AI076423NIAID NIH HHS R01-AI076423
6 · The paper itself

Abstract

Mutations in the Trex1 are associated with a spectrum of type I IFN-dependent autoimmune diseases. Trex1 plays an essential role in preventing accumulation of excessive cytoplasmic DNA, avoiding cell-intrinsic innate DNA sensor activation and suppressing activation of type I IFN-stimulated and -independent antiviral genes. Trex1 also helps HIV to escape cytoplasmic detection by DNA sensors. However, regulation of Trex1 in innate immune cells remains elusive. We report that murine cDCs have high constitutive expression of Trex1 in vitro and in vivo in the spleen. In resting bone marrow-derived cDCs, type I IFNs up-regulate Trex1 expression via the IFNAR-mediated signaling pathway (STAT1- and STAT2-dependent). DC activation induced by TLR3, -4, -7, and -9 ligands also augments Trex1 expression through autocrine IFN-β production and triggering of the IFN signaling pathway, whereas TLR4 ligand LPS also stimulates an early expression of Trex1 through IFN-independent NF-κB-dependent signaling pathway. Furthermore, retroviral infection also induces Trex1 up-regulation in cDCs, as we found that a gene therapy HIV-1-based lentiviral vector induces significant Trex1 expression, suggesting that Trex1 may affect local and systemic administration of gene-therapy vehicles. Our data indicate that Trex1 is induced in cDCs during activation upon IFN and TLR stimulation through the canonical IFN signaling pathway and suggest that Trex1 may play a role in DC activation during infection and autoimmunity. Finally, these results suggest that HIV-like viruses may up-regulate Trex1 to increase their ability to escape immunosurveillance.

Indexed as

Signal TransductionUp-RegulationAnimalsAutocrine CommunicationDendritic CellsExodeoxyribonucleasesGenetic TherapyGenetic VectorsHIV-1HIV InfectionsInterferon-betaLigandsMiceMice, KnockoutNF-kappa BPhosphoproteinsExodeoxyribonucleasesInterferon-betaLigandsNF-kappa BPhosphoproteinsStat1 protein, mouseSTAT1 Transcription FactorStat2 protein, mouseSTAT2 Transcription Factorthree prime repair exonuclease 1Toll-Like Receptorsautoimmunityimmune activationviral infection

Identifiers

PMID24598055
PMCPMC4056275
OpenAlexW2150444151

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.