ArticleThe Journal of biological chemistry2012
Hydrogen sulfide is an endogenous potentiator of T cell activation.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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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.
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Who cites it
72 citing papers in PubMed.
- Significance of GSH and HRedox report : communications in free radical research · 2026Review
- CD47 and FOXP3Cancers · 2026Review
- Reactive sulfur species as emerging immunomodulators: mechanistic insights and therapeutic prospects.Frontiers in immunology · 2026Review
- CD47-mediated tumor microenvironment remodeling: a central mechanism in immune evasion.Acta biochimica et biophysica Sinica · 2025Review
- Hydrogen Sulfide Expression May Affect Ovarian Cancer Progression and Drug Resistance.International journal of women's health · 2025Article
- Cystathionine γ-lyase-derived HActa pharmacologica Sinica · 2024Article
- The reverse transsulfuration pathway affects the colonic microbiota and contributes to colitis in mice.Amino acids · 2024Article
- Interactions between Dietary Antioxidants, Dietary Fiber and the Gut Microbiome: Their Putative Role in Inflammation and Cancer.International journal of molecular sciences · 2024Review
- Dietary methionine restriction in cancer development and antitumor immunity.Trends in endocrinology and metabolism: TEM · 2024Review
- Hydrogen Sulfide: Physiological Roles and Therapeutic Implications against COVID-19.Current medicinal chemistry · 2024Review
- Sepsis-Induced Inhibition of Contractile Function of Lymphatic Nodes.Bulletin of experimental biology and medicine · 2024Article
- Methionine and HNature metabolism · 2023Article
- The Triple Crown: NO, CO, and HPharmacology & therapeutics · 2023Review
- Methionine restriction-induced sulfur deficiency impairs antitumour immunity partially through gut microbiota.Nature metabolism · 2023Article
- Who is in the driver's seat? Parvimonas micra: An understudied pathobiont at the crossroads of dysbiotic disease and cancer.Environmental microbiology reports · 2023Review
- HBiomedicines · 2023Article
- A Reciprocal Link between Oral, Gut Microbiota during Periodontitis: The Potential Role of Probiotics in Reducing Dysbiosis-Induced Inflammation.International journal of molecular sciences · 2023Review
- Microbial metabolites are involved in tumorigenesis and development by regulating immune responses.Frontiers in immunology · 2023Review
- The Role of Hydrogen Sulfide in Plaque Stability.Antioxidants (Basel, Switzerland) · 2022Review
- CD47 interactions with exportin-1 limit the targeting of mJournal of cell communication and signaling · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
H(2)S is an endogenous signaling molecule that may act via protein sulfhydrylation to regulate various physiological functions. H(2)S is also a byproduct of dietary sulfate metabolism by gut bacteria. Inflammatory bowel diseases such as ulcerative colitis are associated with an increase in the colonization of the intestine by sulfate reducing bacteria along with an increase in H(2)S production. Consistent with its increased production, H(2)S is implicated as a mediator of ulcerative colitis both in its genesis or maintenance. As T cells are well established mediators of inflammatory bowel disease, we investigated the effect of H(2)S exposure on T cell activation. Using primary mouse T lymphocytes (CD3+), OT-II CD4+ T cells, and the human Jurkat T cell line, we show that physiological levels of H(2)S potentiate TCR-induced activation. Nanomolar levels of H(2)S (50-500 nM) enhance T cell activation assessed by CD69 expression, interleukin-2 expression, and CD25 levels. Exposure of T cells to H(2)S dose-dependently enhances TCR-stimulated proliferation with a maximum at 300 nM (30% increase, p < 0.01). Furthermore, activation increases the capacity of T cells to make H(2)S via increased expression of cystathionine γ-lyase and cystathionine β-synthase. Disrupting this response by silencing these H(2)S producing enzymes impairs T cell activation, and proliferation and can be rescued by the addition of 300 nM H(2)S. Thus, H(2)S represents a novel autocrine immunomodulatory molecule in T cells.
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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.