Evidence map›Paper›PMID 36923406›Full record

ArticleFrontiers in immunology2023

The STING/TBK1/IRF3/IFN type I pathway is defective in cystic fibrosis.

Luca Occhigrossi, Federica Rossin, Valeria Rachela Villella, Speranza Esposito, Carlo Abbate, Manuela D'Eletto, Maria Grazia Farrace, Antonella Tosco, Roberta Nardacci, Gian Maria Fimia and 2 more

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In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Genetic and chemical correction of cystic fibrosis reduces airway susceptibility to SARS-CoV-2.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  3. Article
  4. Article
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

12 authors at 5 institutions in 1 country.

Luca OcchigrossiDepartment of Epidemiology, Preclinical Research and Advanced Diagnostics, National Institute for Infectious Diseases IRCCS 'L, Spallanzani', Rome, Italy.
Federica RossinDepartment of Biology, University of Rome 'Tor Vergata', Rome, Italy.
Valeria Rachela VillellaEuropean Institute for Research in Cystic Fibrosis, at National Institute for Infectious Diseases IRCCS 'L, Spallanzani', Rome, Italy.
Speranza EspositoEuropean Institute for Research in Cystic Fibrosis, at National Institute for Infectious Diseases IRCCS 'L, Spallanzani', Rome, Italy.
Carlo AbbateDepartment of Biology, University of Rome 'Tor Vergata', Rome, Italy.
Manuela D'ElettoDepartment of Biology, University of Rome 'Tor Vergata', Rome, Italy.
Maria Grazia FarraceDepartment of Biology, University of Rome 'Tor Vergata', Rome, Italy.
Antonella ToscoPediatric Unit, Department of Translational Medical Sciences, Regional Cystic Fibrosis Center, Federico II University Naples, Naples, Italy.
Roberta NardacciDepartment of Epidemiology, Preclinical Research and Advanced Diagnostics, National Institute for Infectious Diseases IRCCS 'L, Spallanzani', Rome, Italy.
Gian Maria FimiaDepartment of Epidemiology, Preclinical Research and Advanced Diagnostics, National Institute for Infectious Diseases IRCCS 'L, Spallanzani', Rome, Italy.
Valeria RaiaEuropean Institute for Research in Cystic Fibrosis, at National Institute for Infectious Diseases IRCCS 'L, Spallanzani', Rome, Italy.
Mauro PiacentiniDepartment of Epidemiology, Preclinical Research and Advanced Diagnostics, National Institute for Infectious Diseases IRCCS 'L, Spallanzani', Rome, Italy.
University of Rome Tor Vergata · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITFederico II University Hospital · ITSaint Camillus International University of Health and Medical Sciences · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis (CF) is a rare autosomal recessive disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The most common mutation is F508del-CFTR (ΔF) which leads the encoded ion channel towards misfolding and premature degradation. The disease is characterized by chronic bronchopulmonary obstruction, inflammation and airways colonization by bacteria, which are the major cause of morbidity and mortality. The STING pathway is the main signaling route activated in the presence of both self and pathogen DNA, leading to Type I Interferon (IFN I) production and the innate immune response. In this study, we show for the first time the relationship existing in CF between resistant and recurrent opportunistic infections by

Indexed as

Cystic FibrosisInterferon Type IAnimalsCystic Fibrosis Transmembrane Conductance RegulatorImmunity, InnateInterferon Regulatory Factor-3MacrophagesMiceProtein Serine-Threonine KinasesCystic Fibrosis Transmembrane Conductance RegulatorInterferon Regulatory Factor-3Interferon Type IIrf3 protein, mouseProtein Serine-Threonine KinasesTbk1 protein, mousebacterial infectionscystic fibrosisinnate immune responseSTING pathwaytype I interferon

Identifiers

PMID36923406
PMCPMC10008931
OpenAlexW4322504000

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read57
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.