Evidence map›Paper›PMID 28615418›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Cutting Edge: Activation of STING in T Cells Induces Type I IFN Responses and Cell Death.

Bridget Larkin, Vladimir Ilyukha, Maxim Sorokin, Anton Buzdin, Edouard Vannier, Alexander Poltorak

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 1% 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

240 citing papers in PubMed, 1 synthesis or guideline pooled it, 344 citations in OpenAlex.

  1. Pooled it
  2. Article
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180 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 5 institutions in 2 countries.

Bridget LarkinProgram in Immunology, Sackler Graduate School, Tufts University, Boston, MA 02111.
Vladimir IlyukhaPetrozavodsk State University, 185910 Petrozavodsk, Republic of Karelia, Russia.ORCID 0000-0002-2371-1740
Maxim SorokinNational Research Centre Kurchatov Institute, Centre for Convergence of Nano-, Bio-Information and Cognitive Sciences and Technologies, Moscow 123182, Russia.
Anton BuzdinD. Rogachyov Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow 117997, Russia.
Edouard VannierDivision of Geographic Medicine and Infectious Diseases, Tufts Medical Center, Boston, MA 02111; and.
Alexander PoltorakProgram in Immunology, Sackler Graduate School, Tufts University, Boston, MA 02111; Alexander.Poltorak@tufts.edu.
Tufts University · USInstitute of Bioorganic Chemistry · RUKurchatov Institute · RUPetrozavodsk State University · RUTufts Medical Center · US

Funding

Hyper-Responsiveness to TLR Agonists in Wild Derived MiceR01AI056234 · NIAID · TUFTS UNIVERSITY BOSTON · PI POLTORAK, ALEXANDER · 2003 to 2023
$8.4M
IMMUNOLOGIC ASPECTS OF DISEASET32AI007077 · NIAID · TUFTS UNIVERSITY BOSTON · PI WORTIS, HENRY H. · 1985 to 2017
$3.5M
Activation of STING-mediated pathway(s) in T cellsR21AI119833 · NIAID · TUFTS UNIVERSITY BOSTON · PI POLTORAK, ALEXANDER · 2016 to 2017
$454k
The regulation of basal interferon and its role in necroptosisR21AI126050 · NIAID · TUFTS UNIVERSITY BOSTON · PI POLTORAK, ALEXANDER · 2016 to 2017
$454k
Understanding genetic basis for resistance to TNF-induced lethal shock using newR21AI090419 · NIAID · TUFTS UNIVERSITY BOSTON · PI POLTORAK, ALEXANDER · 2010 to 2011
$451k
Hyper-Responsiveness to TLR Agonists in Wild Derived MiceR56AI056234 · NIAID · TUFTS UNIVERSITY BOSTON · PI POLTORAK, ALEXANDER · 2008 to 2008
$411k
NIAID NIH HHS R01 AI056234NIAID NIH HHS R21 AI090419NIAID NIH HHS R21 AI119833NIAID NIH HHS R21 AI126050NIAID NIH HHS R56 AI056234NIAID NIH HHS T32 AI007077
6 · The paper itself

Abstract

Stimulator of interferon genes (STING) was initially described as a sensor of intracellular bacterial and viral DNA and a promising adjuvant target in innate immune cells; more recently STING has also been shown to detect endogenous DNA and play a role in tumor immunity and autoimmune disease development. Thus far STING has been studied in macrophages and dendritic cells. In this study, to our knowledge we provide the first evidence of STING activation in T cells, in which STING agonists not only provoke type I IFN production and IFN-stimulated gene expression, mirroring the response of innate cells, but are also capable of activating cell stress and death pathways. Our results suggest a re-evaluation of STING agonist-based therapies may be necessary to identify the possible effects on the T cell compartment. Conversely, the effects of STING on T cells could potentially be harnessed for therapeutic applications.

Indexed as

Cell DeathAnimalsEndoplasmic Reticulum StressImmunity, InnateInterferon Type ILymphocyte ActivationMacrophagesMembrane ProteinsMiceSequence Analysis, RNASTING ProteinT-LymphocytesInterferon Type IMembrane ProteinsSting1 protein, mouseSTING Protein

Identifiers

PMID28615418
PMCPMC5525333
OpenAlexW2626019299

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.