Evidence map›Paper›PMID 28295214›Full record

ReviewEuropean journal of immunology2017

Negative regulators of the RIG-I-like receptor signaling pathway.

Kendra M Quicke, Michael S Diamond, Mehul S Suthar

Open access · bronzeAbstract readReview
In one paragraph

Review in European journal of immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
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  4. Review
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  10. Review
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  12. Immune mechanism ofFrontiers in immunology · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. High RIG-I and EFTUD2 expression predicts poor survival in endometrial cancer.Journal of cancer research and clinical oncology · 2023
    Article
  18. Article
  19. Article
  20. Article

2 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

3 authors at 2 institutions in 1 country.

Kendra M QuickeDivision of Infectious Diseases, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
Michael S DiamondDepartment of Medicine, Washington University School of Medicine, St. Louis, MO, USA.
Mehul S SutharDivision of Infectious Diseases, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
Oregon National Primate Research Center · USWashington University in St. Louis · US

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
Systems Biological Analysis of Innate and Adaptive Responses to VaccinationU19AI090023 · NIAID · EMORY UNIVERSITY · PI AHMED, RAFI, LI, SHUZHAO · 2010 to 2021
$45.0M
West Nile Virus and host control of innate defensesU19AI083019 · NIAID · UNIVERSITY OF WASHINGTON · PI SUTHAR, MEHUL SHAMAL · 2009 to 2018
$22.5M
Innate Immune Control of West Nile VirusR01AI104002 · NIAID · UNIVERSITY OF WASHINGTON · PI DIAMOND, MICHAEL S, GALE, MICHAEL · 2013 to 2017
$3.7M
Emory R38 Research Training ProgramR38AI140299 · NIAID · EMORY UNIVERSITY · PI OFOTOKUN, IGHOVWERHA, ROUPHAEL, NADINE GEORGES · 2018 to 2021
$1.4M
Cell-Specific Programs of Host Defense Against West Nile VirusR01AI074973 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL · 2009 to 2010
$774k
Identifying host genetic determinants that regulate dendritic cell activationR21AI113485 · NIAID · EMORY UNIVERSITY · PI SUTHAR, MEHUL SHAMAL · 2015 to 2016
$494k
Regulation of T cell immunity by the cytosolic RIG-I like receptorsR56AI110516 · NIAID · EMORY UNIVERSITY · PI SUTHAR, MEHUL SHAMAL · 2014 to 2014
$443k
NIAID NIH HHS R01 AI074973NIAID NIH HHS R01 AI104002NIAID NIH HHS R21 AI113485NIAID NIH HHS R38 AI140299NIAID NIH HHS R56 AI110516NIAID NIH HHS U19 AI083019NIAID NIH HHS U19 AI090023NIH HHS P51 OD011132
6 · The paper itself

Abstract

Upon recognition of specific molecular patterns on microbes, host cells trigger an innate immune response, which culminates in the production of type I interferons, proinflammatory cytokines and chemokines, and restricts pathogen replication and spread within the host. At each stage of this response, there are stimulatory and inhibitory signals that regulate the magnitude, quality, and character of the response. Positive regulation promotes an antiviral state to control and eventually clear infection, whereas negative regulation dampens inflammation and prevents immune-mediated tissue damage. An overexuberant innate response can lead to cell and tissue destruction, and the development of spontaneous autoimmunity. The retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), RIG-I and melanoma differentiation-associated gene 5 (MDA5), belong to a family of cytosolic host RNA helicases that recognize distinct nonself RNA signatures and trigger innate immune responses against several RNA viruses by signaling through the essential adaptor protein mitochondrial antiviral signaling (MAVS). The RLR signaling pathway is tightly regulated to maximize antiviral immunity and minimize immune-mediated pathology. This review highlights contemporary findings on negative regulators of the RLR signaling pathway, with specific focus on the proteins and biological processes that directly regulate RIG-I, MDA5 and MAVS signaling function.

Indexed as

Immunity, InnateAdaptor Proteins, Signal TransducingAnimalsDEAD Box Protein 58Feedback, PhysiologicalHost-Pathogen InteractionsHumansInflammationInterferon-Induced Helicase, IFIH1RNASignal TransductionVirus DiseasesAdaptor Proteins, Signal TransducingDEAD Box Protein 58IFIH1 protein, humanInterferon-Induced Helicase, IFIH1MAVS protein, humanRNAInnate responseMAVSMDA5Negative regulationRIG-I

Identifiers

PMID28295214
PMCPMC5554756
OpenAlexW2592208529

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.