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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Citations
Cites
1 retracted
D’Souza, A. D., Parish, I. A., McKay, S. E., Kaech, S. M., & Shadel, G. S. (2011) · American Journal Of Pathology · doi:10.1016/j.ajpath.2011.02.022 · Cited by 11
RetractedCellular mechanisms and physiological consequences of redox-dependent signalling
Holmström, K. M., & Finkel, T. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3801 · Cited by 2,093
Metabolic Pathways in Immune Cell Activation and Quiescence
Pearce, E. L., & Pearce, E. J. (2013) · Immunity · doi:10.1016/j.immuni.2013.04.005 · Cited by 1,692
Fueling Immunity: Insights into Metabolism and Lymphocyte Function
Pearce, E. L., Poffenberger, M. C., Chang, C.-H., & Jones, R. G. (2013) · Science · doi:10.1126/science.1242454 · Cited by 1,363
Metabolic Regulation of T Lymphocytes
MacIver, N. J., Michalek, R. D., & Rathmell, J. C. (2013) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032712-095956 · Cited by 1,244
Delgoffe, G. M., Pollizzi, K. N., Waickman, A. T., Heikamp, E., Meyers, D. J., Horton, M. R., Xiao, B., Worley, P. F., & Powell, J. D. (2011) · Nature Immunology · doi:10.1038/ni.2005 · Cited by 1,141
ATM Activation by Oxidative Stress
Guo, Z., Kozlov, S., Lavin, M. F., Person, M. D., & Paull, T. T. (2010) · Science · doi:10.1126/science.1192912 · Cited by 1,079
Mitochondria in the Regulation of Innate and Adaptive Immunity
Weinberg, S. E., Sena, L. A., & Chandel, N. S. (2015) · Immunity · doi:10.1016/j.immuni.2015.02.002 · Cited by 960
Metabolic programming and PDHK1 control CD4+ T cell subsets and inflammation
Gerriets, V. A., Kishton, R. J., Nichols, A., Macintyre, A. N., Inoue, M., Ilkayeva, O., Winter, P. S., Liu, X., Priyadharshini, B., Slawinska, M. E., et al. (2014) · Journal of Clinical Investigation · doi:10.1172/jci76012 · Cited by 747
The Energy Sensor AMPK Regulates T Cell Metabolic Adaptation and Effector Responses In Vivo
Blagih, J., Coulombe, F., Vincent, E. E., Dupuy, F., Galicia-Vázquez, G., Yurchenko, E., Raissi, T. C., van der Windt, G. J. W., Viollet, B., Pearce, E. L., et al. (2015) · Immunity · doi:10.1016/j.immuni.2014.12.030 · Cited by 679
Cited by
Sorted by citations
Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies
Guo, Q., Wang, Y., Xu, D., Nossent, J. C., Pavlos, N. J., & Xu, J. (2018) · Bone Research · doi:10.1038/s41413-018-0016-9 · Cited by 1,829
Immunopathogenesis of Rheumatoid Arthritis
Firestein, G. S., & McInnes, I. B. (2017) · Immunity · doi:10.1016/j.immuni.2017.02.006 · Cited by 1,301
Lactate modulation of immune responses in inflammatory versus tumour microenvironments
Certo, M., Tsai, C.-H., Pucino, V., Ho, P.-C., & Mauro, C. (2021) · Nature Reviews Immunology · doi:10.1038/s41577-020-0406-2 · Cited by 924
Metabolism of immune cells in cancer
Leone, R. D., & Powell, J. D. (2020) · Nature Reviews Cancer · doi:10.1038/s41568-020-0273-y · Cited by 877
The immunology of rheumatoid arthritis
Weyand, C. M., & Goronzy, J. J. (2020) · Nature Immunology · doi:10.1038/s41590-020-00816-x · Cited by 835
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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