The DOI matches its Crossref record; 44 of the 45 references it cites were found in a registry or an index.
Restoring oxidant signaling suppresses proarthritogenic T cell effector functions in rheumatoid arthritis
Open accessAbstract
ROS deficiency promotes proinflammatory T cells in rheumatoid arthritis.
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In the citing paper
“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
In the citing paper
“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
In the citing paper
“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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Self-citation
Metadata
- 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
- PMC
- PMC5074090
- 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
- green
- www.ncbi.nlm.nih.gov
- 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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