Evidence map›Paper›PMID 25747479›Full record

ArticleMethods in enzymology2015

CD47-dependent regulation of H₂S biosynthesis and signaling in T cells.

Sukhbir Kaur, Anthony L Schwartz, Thomas W Miller, David D Roberts

Open access · greenAbstract read
In one paragraph

Article in Methods in enzymology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
9.3field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. CD47 and FOXP3Cancers · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. SPRC Suppresses Experimental Periodontitis by Modulating Th17/Treg Imbalance.Frontiers in bioengineering and biotechnology · 2021
    Article
  11. Hydrogen Sulfide and the Immune System.Advances in experimental medicine and biology · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Blocking CD47-SIRPα Signal Axis as Promising Immunotherapy in Ovarian Cancer.Cancer control : journal of the Moffitt Cancer Center
    Review
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.

Sukhbir KaurLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Anthony L SchwartzLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Thomas W MillerLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
David D RobertsLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: droberts@helix.nih.gov.
National Institutes of Health · US

Funding

Cellular Interactions with ThrombospondinZIASC009172 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$17.9M
Intramural NIH HHS ZIA SC009172
6 · The paper itself

Abstract

Pharmacological concentrations of H2S donors inhibit some T cell functions by inhibiting mitochondrial function, but evidence is also emerging that H2S at physiological concentrations produced via chemical sources and endogenously is a positive physiological mediator of T cell function. Expression of the H2S biosynthetic enzymes cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) is induced in response to T cell receptor signaling. Inhibiting the induction of these enzymes limits T cell activation and proliferation, which can be overcome by exposure to exogenous H2S at submicromolar concentrations. Exogenous H2S at physiological concentrations increases the ability of T cells to form an immunological synapse by altering cytoskeletal actin dynamics and increasing the reorientation of the microtubule-organizing center. Downstream, H2S enhances T cell receptor-dependent induction of CD69, CD25, and Interleukin-2 (IL-2) gene expression. The T cell stimulatory activity of H2S is enhanced under hypoxic conditions that limit its oxidative metabolism by mitochondrial and nonenzymatic processes. Studies of the receptor CD47 have revealed the first endogenous inhibitory signaling pathway that regulates H2S signaling in T cells. Binding of the secreted protein thrombospondin-1 to CD47 elicits signals that block the stimulatory activity of exogenous H2S on T cell activation and limit the induction of CSE and CBS gene expression. CD47 signaling thereby inhibits T cell receptor-mediated T cell activation.

Indexed as

Acute Kidney InjuryAnimalsAnti-Inflammatory Agents, Non-SteroidalArthritis, RheumatoidAsthmaCD47 AntigenCell AdhesionCell ProliferationCystathionine beta-SynthaseCystathionine gamma-LyaseGene Expression RegulationHumansHydrogen SulfideImmunity, CellularImmunological SynapsesInflammationAnti-Inflammatory Agents, Non-SteroidalCD47 AntigenCystathionine beta-SynthaseCystathionine gamma-LyaseHydrogen SulfideThrombospondin 1CD47Cystathionine β-synthaseCystathionine γ-lyaseHydrogen sulfideInflammationT-cell activationT-cell receptorThrombospondin-1

Identifiers

PMID25747479
PMCPMC7738002
OpenAlexW38497621

What OpenQuestion holds

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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.