Cited by 282Rheumatoid Arthritis Research and TherapiesRedox biology and oxidative stressT-cell and B-cell Immunology

Restoring oxidant signaling suppresses proarthritogenic T cell effector functions in rheumatoid arthritis

Open access
Yang, Zhen, Shen, Yi, Oishi, Hisashi, Matteson, Eric L., Tian, Lu, Goronzy, Jörg J., Weyand, Cornelia M.·2016·Science Translational Medicine

Abstract

ROS deficiency promotes proinflammatory T cells in rheumatoid arthritis.

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Crossref · 10.1126/scitranslmed.aad7151

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44 of 44 references verified0 citation errors · 0 not checkable

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  • RA naive CD4+ T cells are constitutively low in intracellular ROS due to metabolic reprogramming and a fundamental shift in glucose utilization.

    “RA naive CD4+ T cells are constitutively low in intracellular ROS due to metabolic reprogramming and a fundamental shift in glucose utilization”

    From Successful and Maladaptive T Cell Aging (2017) · cites this paper as Yang et al., 2016

  • ATM loss biases T cells to shift their differentiation pattern to a preferential commitment for the Th1 and Th17 cell lineages.

    “ATM loss biases T cells to shift their differentiation pattern to a preferential commitment for the Th1 and Th17 cell lineages”

    From Successful and Maladaptive T Cell Aging (2017) · cites this paper as Yang et al., 2016

  • Due to reduced production of glycolytic enzyme PFKFB3 and upregulation of G6PD, RA T cells shunt glucose toward the pentose phosphate pathway, switching from catabolic to synthetic metabolism.

    “Due to reduced production of the glycolytic enzyme PFKFB3 and the upregulation of G6PD, RA T cells shunt glucose toward the pentose phosphate pathway, switching from a catabolic to a synthetic metabolism”

    From Successful and Maladaptive T Cell Aging (2017) · cites this paper as Yang et al., 2016

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1 retracted

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Authors
Yang, Z., Shen, Y., Oishi, H., Matteson, E. L., Tian, L., Goronzy, J. J., & Weyand, C. M.
Affiliations
  • Stanford Medicine (US)
  • Mayo Clinic (US)
  • Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA 94305, USA.
Corresponding author
Weyand, Cornelia M.
Venue
Science Translational Medicine
Published
2016-03-23
Volume
8
Issue
331
Pages
331ra38-331ra38
ISSN
  • 1946-6234 (ISSN-L)
  • 1946-6242
OpenAlex
W2309229101
Cited by
275
References
45
Citations by year
2026: 22 · 2025: 19 · 2024: 29 · 2023: 23 · 2022: 29 · 2021: 35 · 2020: 32 · 2019: 27 · 2018: 24 · 2017: 24 · 2016: 11
FWCI
30.50
Type
journal article
Language
en
Open access
Locations
  • Science Translational Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • NIH (AR042527, AI044142, AI108906, HL058000, AI108891, AG045779)
  • Govenar Discovery Fund
  • Northern California Arthritis Foundation
Topics
  • Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
rheumatoid arthritis, CD4+ T cells, T cell hyperproliferation, glucose-6-phosphate dehydrogenase, pentose phosphate pathway, glycolysis, NADPH, reactive oxygen species, oxidant signaling, ATM kinase, G2/M checkpoint, Th1 differentiation, Th17 cell differentiation, synovitis, autoimmunity, T cell metabolism
MeSH terms
Arthritis, Rheumatoid, Cell Differentiation, Glucose, Glutathione, Humans, Inflammation, NADP, Oxidation-Reduction, Pentose Phosphate Pathway, Stress, Physiological, T-Lymphocytes, Signal Transduction, Free Radical Scavengers, Oxidants, Reactive Oxygen Species, Cell Proliferation, Cell Cycle Checkpoints, Ataxia Telangiectasia Mutated Proteins

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