ArticleImmunity2013
Mitochondria are required for antigen-specific T cell activation through reactive oxygen species signaling.
Article in Immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 818 papers.
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.
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.
Who cites it
818 citing papers in PubMed, 1,261 citations in OpenAlex.
- The mitochondrial chaperone HSPD1 folds MTHFD2 independently of its co-chaperone HSPE1.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Mitochondrial transfer-driven immune evasion in the tumor microenvironment.International immunology · 2026Review
- Targeting the HPGDS-PGDSignal transduction and targeted therapy · 2026Article
- Glioma microenvironment: Cellular crosstalk, immunosuppression, and novel therapeutic perspectives.Chinese medical journal · 2026Review
- Epigenetic training licenses naïve CD8Science advances · 2026Article
- Boosting T cell antioxidant capacity: A strategic approach to overcome immunosuppression in solid tumors.Redox biology · 2026Review
- Metabolomics of in vivo inflammation identifies soluble sialic acid as a conserved myeloid-cell metabolite.The Journal of biological chemistry · 2026Article
- Immunomodulatory Nanozymes as Programmable Redox-Immune Set-Point Regulators.Small (Weinheim an der Bergstrasse, Germany) · 2026Review
- Article
- Unconventional role of hydroxymethylglutaryl-CoA synthase 1 in driving pathogenic TScience advances · 2026Article
- Ferroptosis in T cells: mechanisms, biology and translational opportunities.Nature reviews. Immunology · 2026Review
- Metabolic rewiring of the dendritic cell-T cell axis: tumour-derived barriers and therapeutic opportunities.Experimental & molecular medicine · 2026Review
- Review
- Review
- Review
- Dysfunctional Mitochondria in Microglia Drive Cognitive Aging and Neurodegeneration via cGAS-STING.Neuroscience bulletin · 2026Article
- Metabolomics ofbioRxiv : the preprint server for biology · 2026Article
- FAS-controlled T cells drive lymphoproliferation through glycolysis without effector differentiation.Journal of human immunity · 2026Article
- Dipeptidyl peptidase 3 sets the threshold for immune activation and survival during experimental bacterial infection.Nature communications · 2026Article
- Therapeutic effects of a synthetic glabridin derivative on metabolic immuno-regulation and salivary gland functional restoration in experimental Sjögren's syndrome.Experimental & molecular medicine · 2026Article
758 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
It is widely appreciated that T cells increase glycolytic flux during activation, but the role of mitochondrial flux is unclear. Here, we have shown that mitochondrial metabolism in the absence of glucose metabolism is sufficient to support interleukin-2 (IL-2) induction. Furthermore, we used mice with reduced mitochondrial reactive oxygen species (mROS) production in T cells (T-Uqcrfs(-/-) mice) to show that mitochondria are required for T cell activation to produce mROS for activation of nuclear factor of activated T cells (NFAT) and subsequent IL-2 induction. These mice could not induce antigen-specific expansion of T cells in vivo, but Uqcrfs1(-/-) T cells retained the ability to proliferate in vivo under lymphopenic conditions. This suggests that Uqcrfs1(-/-) T cells were not lacking bioenergetically but rather lacked specific ROS-dependent signaling events needed for antigen-specific expansion. Thus, mitochondrial metabolism is a critical component of T cell activation through the production of complex III ROS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.