Evidence map›Paper›PMID 30487791›Full record

ArticleFrontiers in immunology2018

Sulforaphane Inhibits Inflammatory Responses of Primary Human T-Cells by Increasing ROS and Depleting Glutathione.

Jie Liang, Beate Jahraus, Emre Balta, Jacqueline D Ziegler, Katrin Hübner, Norbert Blank, Beate Niesler, Guido H Wabnitz, Yvonne Samstag

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 76 citations in OpenAlex.

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  13. The Multifaceted Roles of NRF2 in Cancer: Friend or Foe?Antioxidants (Basel, Switzerland) · 2024
    Review
  14. Review
  15. What nature has to offer: Opportunities for immuno-oncology.Journal of food and drug analysis · 2023
    Review
  16. Mechanistic review of sulforaphane as a chemoprotective agent in bladder cancer.American journal of clinical and experimental urology · 2023
    Review
  17. Article
  18. Immunomodulatory Effects of (Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  19. Review
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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

9 authors at 1 institution in 1 country.

Jie LiangSection Molecular Immunology, Institute of Immunology, Heidelberg University, Heidelberg, Germany.
Beate JahrausSection Molecular Immunology, Institute of Immunology, Heidelberg University, Heidelberg, Germany.
Emre BaltaSection Molecular Immunology, Institute of Immunology, Heidelberg University, Heidelberg, Germany.
Jacqueline D ZieglerSection Molecular Immunology, Institute of Immunology, Heidelberg University, Heidelberg, Germany.
Katrin HübnerSection Molecular Immunology, Institute of Immunology, Heidelberg University, Heidelberg, Germany.
Norbert BlankDivision of Rheumatology, Department of Internal Medicine V, Heidelberg University, Heidelberg, Germany.
Beate NieslerDepartment of Human Molecular Genetics, Heidelberg University, Heidelberg, Germany.
Guido H WabnitzSection Molecular Immunology, Institute of Immunology, Heidelberg University, Heidelberg, Germany.
Yvonne SamstagSection Molecular Immunology, Institute of Immunology, Heidelberg University, Heidelberg, Germany.
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activity and function of T-cells are influenced by the intra- and extracellular redox milieu. Oxidative stress induces hypo responsiveness of untransformed T-cells. Vice versa increased glutathione (GSH) levels or decreased levels of reactive oxygen species (ROS) prime T-cell metabolism for inflammation, e.g., in rheumatoid arthritis. Therefore, balancing the T-cell redox milieu may represent a promising new option for therapeutic immune modulation. Here we show that sulforaphane (SFN), a compound derived from plants of the Brassicaceae family, e.g., broccoli, induces a pro-oxidative state in untransformed human T-cells of healthy donors or RA patients. This manifested as an increase of intracellular ROS and a marked decrease of GSH. Consistently, increased global cysteine sulfenylation was detected. Importantly, a major target for SFN-mediated protein oxidation was STAT3, a transcription factor involved in the regulation of T

Indexed as

Anti-Inflammatory AgentsArthritis, RheumatoidBrassicaceaeCells, CulturedDown-RegulationGlutathioneHumansImmunosuppression TherapyInflammationInterleukin-17Interleukin-22InterleukinsIsothiocyanatesNuclear Receptor Subfamily 1, Group F, Member 3Primary Cell CultureReactive Oxygen SpeciesAnti-Inflammatory AgentsGlutathioneInterleukin-17Interleukin-22InterleukinsIsothiocyanatesNuclear Receptor Subfamily 1, Group F, Member 3Reactive Oxygen SpeciesSTAT3 Transcription FactorsulforaphaneSulfoxidesglutathioneprimary human T-cellsreactive oxygen speciesrheumatoid arthritissulforaphaneTH17

Identifiers

PMID30487791
PMCPMC6246742
OpenAlexW2901842078

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.