Evidence map›Paper›PMID 22938635›Full record

ReviewAntioxidants & redox signaling2013

Redox regulation of T-cell function: from molecular mechanisms to significance in human health and disease.

Pravin Kesarwani, Anuradha K Murali, Amir A Al-Khami, Shikhar Mehrotra

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

129 citing papers in PubMed, 218 citations in OpenAlex.

  1. Trial
  2. Immunomodulatory Nanozymes as Programmable Redox-Immune Set-Point Regulators.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
  3. Article
  4. On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Contrasting the genetic architecture of cardiac glutathione against other organs: unveiling a unique tissue-specific locus.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  9. Review
  10. Review
  11. Article
  12. Macrophage ferroptosis in hematologic malignancies: emerging mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

69 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Pravin KesarwaniDepartment of Surgery, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Anuradha K Murali
Amir A Al-Khami
Shikhar Mehrotra
Medical University of South Carolina · US

Funding

Oxidative stress and AICD in memory T cell persistenceR01CA138930 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MEHROTRA, SHIKHAR · 2010 to 2014
$1.5M
NCI NIH HHS R01CA138930
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are thought to have effects on T-cell function and proliferation. Low concentrations of ROS in T cells are a prerequisite for cell survival, and increased ROS accumulation can lead to apoptosis/necrosis. The cellular redox state of a T cell can also affect T-cell receptor signaling, skewing the immune response. Various T-cell subsets have different redox statuses, and this differential ROS susceptibility could modulate the outcome of an immune response in various disease states. Recent advances in T-cell redox signaling reveal that ROS modulate signaling cascades such as the mitogen-activated protein kinase, phosphoinositide 3-kinase (PI3K)/AKT, and JAK/STAT pathways. Also, tumor microenvironments, chronic T-cell stimulation leading to replicative senescence, gender, and age affect T-cell susceptibility to ROS, thereby contributing to diverse immune outcomes. Antioxidants such as glutathione, thioredoxin, superoxide dismutase, and catalase balance cellular oxidative stress. T-cell redox states are also regulated by expression of various vitamins and dietary compounds. Changes in T-cell redox regulation may affect the pathogenesis of various human diseases. Many strategies to control oxidative stress have been employed for various diseases, including the use of active antioxidants from dietary products and pharmacologic or genetic engineering of antioxidant genes in T cells. Here, we discuss the existence of a complex web of molecules/factors that exogenously or endogenously affect oxidants, and we relate these molecules to potential therapeutics.

Indexed as

Oxidative StressAnimalsAutoimmune DiseasesCardiovascular DiseasesGene Expression RegulationHealthHumansInflammationMAP Kinase Signaling SystemMitogen-Activated Protein KinasesNeoplasmsOxidation-ReductionParkinson DiseaseSkin DiseasesT-LymphocytesTranscription FactorsMitogen-Activated Protein KinasesTranscription Factors

Identifiers

PMID22938635
PMCPMC3603502
OpenAlexW2147299173

What OpenQuestion holds

Textmetadata
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.