Evidence map›Paper›PMID 29524605›Full record

ReviewFree radical biology & medicine2018

Redox-sensitive signaling in inflammatory T cells and in autoimmune disease.

Cornelia M Weyand, Yi Shen, Jorg J Goronzy

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Reductive stress in cancer immunology and targeted therapy.Acta biochimica et biophysica Sinica · 2026
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  18. Malabaricone C, a constituent of spiceJournal of biosciences · 2023
    Article
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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

3 authors at 2 institutions in 1 country.

Cornelia M WeyandDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA; Department of Medicine, Veterans Affairs Palo Alto Health Care System Palo Alto, CA 94306, USA. Electronic address: cweyand@stanford.edu.
Yi ShenDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA; Department of Medicine, Veterans Affairs Palo Alto Health Care System Palo Alto, CA 94306, USA.
Jorg J GoronzyDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA; Department of Medicine, Veterans Affairs Palo Alto Health Care System Palo Alto, CA 94306, USA.
Stanford University · USVA Palo Alto Health Care System · US

Funding

VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
The Role of Inflammation in Cardiovascular DiseaseP01HL129941 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNSTEIN, KENNETH E · 2016 to 2020
$12.4M
The NOTCH Signaling Pathway in Large Vessel VasculitisR01HL117913 · NHLBI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2025
$5.0M
Oligoclonal T Cell Expansion &Rheumatoid ArthritisR01AR042527 · NIAMS · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1993 to 2022
$4.8M
microRNA Regulation of T Cell SenescenceR01AI108891 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2014 to 2023
$4.6M
Telomere Damage Responses and Immune AgingR01AI108906 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2024
$4.0M
Influence of Age on CD4 T Memory CellsR01AG045779 · NIA · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2013 to 2023
$4.0M
T Cell Signaling in Rheumatoid ArthritisI01BX001669 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI GORONZY, JORG J · 2012 to 2021
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BLRD VA I01 BX001669NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R01 HL117913NIAID NIH HHS R01 AI108891NIAID NIH HHS R01 AI108906NIAID NIH HHS U19 AI057266NIAMS NIH HHS R01 AR042527NIA NIH HHS R01 AG045779
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are byproducts of oxygen metabolism best known for their damaging potential, but recent evidence has exposed their role as secondary messengers, which regulate cell function through redox-activatable signaling systems. In immune cells, specifically in T cells, redox-sensitive signaling pathways have been implicated in controlling several functional domains; including cell cycle progression, T effector cell differentiation, tissue invasion and inflammatory behavior. T cells from patients with the autoimmune disease rheumatoid arthritis (RA) have emerged as a valuable model system to examine the functional impact of ROS on T cell function. Notably, RA T cells are distinguished from healthy T cells based on reduced ROS production and undergo "reductive stress". Upstream defects leading to the ROS

Indexed as

Oxidative StressAnimalsAutoimmune DiseasesHumansInflammationOxidation-ReductionReactive Oxygen SpeciesSignal TransductionT-LymphocytesReactive Oxygen SpeciesATMGlycolysisNADPHPodosomesReactive oxygen speciesReductive stressRheumatoid arthritisTissue invasionTKS5

Identifiers

PMID29524605
PMCPMC6128787
OpenAlexW2793212599

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.