Evidence map›Paper›PMID 25385820›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

STING-mediated DNA sensing promotes antitumor and autoimmune responses to dying cells.

Jared Klarquist, Cassandra M Hennies, Maria A Lehn, Rachel A Reboulet, Sonia Feau, Edith M Janssen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 1 pooled it
5.9field-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

133 citing papers in PubMed, 1 synthesis or guideline pooled it, 200 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  5. Review
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  8. Review
  9. A PI(3,5)PNature communications · 2026
    Article
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  11. Article
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  15. Article
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  18. Article
  19. Cell biological insights into human STING variants.Cell structure and function · 2025
    Review
  20. Article

73 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

6 authors at 3 institutions in 1 country.

Jared KlarquistDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229; and.
Cassandra M HenniesDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229; and.
Maria A LehnDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229; and.
Rachel A RebouletDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229; and.
Sonia FeauDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037.
Edith M JanssenDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229; and Edith.Janssen@cchmc.org.
University of Cincinnati · USCincinnati Children's Hospital Medical Center · USLa Jolla Institute for Immunology · US

Funding

ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI FLICK, MATTHEW J. · 2001 to 2015
$9.2M
Activating robust immunity to tumor-associated antigens:mechanisms and biologyR01CA138617 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI JANSSEN, EDITH M · 2009 to 2013
$1.5M
Dendritic Cells in the Breaking of Peripheral Tolerance in Type 1 DiabetesR01DK090978 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI JANSSEN, EDITH M, KATZ, JONATHAN DAVID · 2010 to 2012
$843k
NCI NIH HHS CA138617NCI NIH HHS R01 CA138617NIAMS NIH HHS P30 AR047363NIDDK NIH HHS DK090978NIDDK NIH HHS R01 DK090978
6 · The paper itself

Abstract

Adaptive immune responses to Ags released by dying cells play a critical role in the development of autoimmunity, allograft rejection, and spontaneous as well as therapy-induced tumor rejection. Although cell death in these situations is considered sterile, various reports have implicated type I IFNs as drivers of the ensuing adaptive immune response to cell-associated Ags. However, the mechanisms that underpin this type I IFN production are poorly defined. In this article, we show that dendritic cells (DCs) can uptake and sense nuclear DNA-associated entities released by dying cells to induce type I IFN. Remarkably, this molecular pathway requires STING, but not TLR or NLR function, and results in the activation of IRF3 in a TBK1-dependent manner. DCs are shown to depend on STING function in vivo to efficiently prime IFN-dependent CD8(+) T cell responses to tumor Ags. Furthermore, loss of STING activity in DCs impairs the generation of follicular Th cells and plasma cells, as well as anti-nuclear Abs, in an inducible model of systemic lupus erythematosus. These findings suggest that the STING pathway could be manipulated to enable the rational design of immunotherapies that enhance or diminish antitumor and autoimmune responses, respectively.

Indexed as

AutoimmunityAnimalsAntigensB-Lymphocyte SubsetsCell DeathDendritic CellsDisease Models, AnimalDNAInterferon Regulatory Factor-3Interferon Type ILupus Erythematosus, SystemicMembrane ProteinsMiceMice, KnockoutNeoplasmsSignal TransductionAntigensDNAInterferon Regulatory Factor-3Interferon Type IMembrane ProteinsSting1 protein, mouseSTING Protein

Identifiers

PMID25385820
PMCPMC4258444
OpenAlexW1630358515

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.