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Cited by 459Redox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative MechanismsT-cell and B-cell Immunology

The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.

Discrete Generation of Superoxide and Hydrogen Peroxide by T Cell Receptor Stimulation

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Devadas, Satish, Zaritskaya, Luba, Rhee, Sue Goo, Oberley, Larry, Williams, Mark S.·2002·The Journal of Experimental Medicine
DOI 10.1084/jem.20010659PMC PMC2196010
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Abstract

Receptor-stimulated generation of reactive oxygen species (ROS) has been shown to regulate signal transduction, and previous studies have suggested that T cell receptor (TCR) signals may involve or be sensitive to ROS. In this study, we have shown for the first time that TCR cross-linking induced rapid (within 15 min) generation of both hydrogen peroxide and superoxide anion, as defined with oxidation-sensitive dyes, selective pharmacologic antioxidants, and overexpression of specific antioxidant enzymes. Furthermore, the data suggest the novel observation that superoxide anion and hydrogen peroxide are produced separately by distinct TCR-stimulated pathways. Unexpectedly, TCR-stimulated activation of the Fas ligand (FasL) promoter and subsequent cell death was dependent upon superoxide anion, but independent of hydrogen peroxide, while nuclear factor of activated T cells (NFAT) activation or interleukin 2 transcription was independent of all ROS. Anti-CD3 induced phosphorylation of extracellular signal–regulated kinase (ERK)1/2 required hydrogen peroxide generation but was unaffected by superoxide anion. Thus, antigen receptor signaling induces generation of discrete species of oxidants that selectively regulate two distinct redox sensitive pathways, a proapoptotic (FasL) and a proliferative pathway (ERK).

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  1. 1992, Adv. Enzymol., 65, 49
  2. 1988, Immunology., 63, 431
  3. 1999, Cancer Res., 59, 6276
  4. 1998, Environ. Health Perspect., 106, 1179

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Metadata

Authors
Devadas, S., Zaritskaya, L., Rhee, S. G., Oberley, L., & Williams, M. S.
Affiliations
  • American Red Cross (US)
  • National Institutes of Health (US)
  • University of Iowa (US)
ORCID
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
2002-01-07
Volume
195
Issue
1
Pages
59-70
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
DOI
10.1084/jem.20010659
PMC
PMC2196010
OpenAlex
W2157579772
Cited by
458
References
59
Citations by year
2026: 11 · 2025: 10 · 2024: 22 · 2023: 10 · 2022: 19 · 2021: 26 · 2020: 29 · 2019: 19 · 2018: 18 · 2017: 21 · 2016: 19 · 2015: 19 · 2014: 21 · 2013: 18 · 2012: 15
FWCI
8.23
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
American Heart Association
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
T cell receptor signaling, reactive oxygen species, superoxide, hydrogen peroxide, T cell activation, apoptosis, NFAT activation, interleukin-2 transcription, ERK1/2 phosphorylation, redox signaling, oxidative stress
MeSH terms
Animals, Humans, Hybridomas, Hydrogen Peroxide, Lymphocyte Activation, Membrane Glycoproteins, Oxidation-Reduction, Peroxides, Receptors, Antigen, T-Cell, Superoxides, T-Lymphocytes, Signal Transduction, Free Radical Scavengers, Apoptosis, CD3 Complex, Reactive Oxygen Species, Models, Immunological, Mitogen-Activated Protein Kinases, Mice, Fas Ligand Protein

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