Evidence map›Paper›PMID 25605286›Full record

ArticleEuropean journal of immunology2015

TGF-β converts Th1 cells into Th17 cells through stimulation of Runx1 expression.

Hou-Pu Liu, Anthony T Cao, Ting Feng, Qingjie Li, Wenbo Zhang, Suxia Yao, Sara M Dann, Charles O Elson, Yingzi Cong

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03615729 (RORC Genetic Polymorphism and Serum Levels in Patients With Rheumatoid Arthritis), which is not on this map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.8field-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.

NCT03615729 completednot on this mapstarted 2016, after this paper: background citation

RORC Genetic Polymorphism and Serum Levels in Patients With Rheumatoid Arthritis

TypeobservationalSponsorAssiut UniversityRan2016 to 2018Enrolled89ConditionsGenetic Predisposition to Disease
3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
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  6. Alteration of mJournal of clinical medicine · 2023
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  10. NF-κB signaling pathway mechanism in cow intertoe skin inflammation caused byFrontiers in cellular and infection microbiology · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Glutaminolysis and CD4Frontiers in immunology · 2022
    Review
  16. Review
  17. Benefits of α-lipoic acid in high-risk pregnancies (Review).Experimental and therapeutic medicine · 2021
    Review
  18. Review
  19. Review
  20. Article
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 2 institutions in 1 country.

Hou-Pu LiuDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, USA.
Anthony T Cao
Ting Feng
Qingjie Li
Wenbo Zhang
Suxia Yao
Sara M Dann
Charles O Elson
Yingzi Cong
The University of Texas Medical Branch at Galveston · USUniversity of Alabama at Birmingham · US

Funding

The role of CBir1 flagellin-specific Th17 and Th1 effector cells in colitisR01DK079918 · NIDDK · UNIVERSITY OF TEXAS MED BR GALVESTON · PI CONG, YINGZI · 2008 to 2012
$1.5M
microRNA-10a Regulation of Inflammatory Bowel DiseasesR01DK098370 · NIDDK · UNIVERSITY OF TEXAS MED BR GALVESTON · PI CONG, YINGZI · 2013 to 2016
$1.3M
NIDDK NIH HHS DK079918NIDDK NIH HHS DK098370NIDDK NIH HHS R01 DK079918NIDDK NIH HHS R01 DK098370
6 · The paper itself

Abstract

Differentiated CD4(+) T cells preserve plasticity under various conditions. However, the stability of Th1 cells is unclear, as is whether Th1 cells can convert into Th17 cells and thereby contribute to the generation of IFN-γ(+) IL-17(+) CD4(+) T cells, the number of which correlates with severity of colitis. We investigated whether IFN-γ(+) Th1 cells can convert into Th17 cells under intestinal inflammation and the mechanisms involved. IFN-γ(Thy1.1+) Th1 cells were generated by culturing naïve CD4(+) T cells from IFN-γ(Thy1.1) CBir1 TCR-Tg reporter mice, whose TCR is specific for an immunodominant microbiota antigen, CBir1 flagellin, under Th1 polarizing conditions. IFN-γ(Thy1.1+) Th1 cells induced colitis in Rag(-/-) mice after adoptive transfer and converted into IL-17(+) Th17, but not Foxp3(+) Treg cells in the inflamed intestines. TGF-β and IL-6, but not IL-1β and IL-23, regulated Th1 conversion into Th17 cells. TGF-β induction of transcriptional factor Runx1 is crucial for the conversion, since silencing Runx1 by siRNA inhibited Th1 conversion into Th17 cells. Furthermore, TGF-β enhanced histone H3K9 acetylation but inhibited H3K9 trimethylation of Runx1- and ROR-γt-binding sites on il-17 or rorc gene in Th1 cells. We conclude that Th1 cells convert into Th17 cells under inflammatory conditions in intestines, which is possibly mediated by TGF-β induction of Runx1.

Indexed as

AcetylationAnimalsBinding SitesCell DifferentiationCells, CulturedColitisCore Binding Factor Alpha 2 SubunitFlagellinHistonesHomeodomain ProteinsInterferon-gammaInterleukin-17Interleukin-1betaInterleukin-2Interleukin-23Interleukin-6CBir1 flagellinCore Binding Factor Alpha 2 SubunitFlagellinHistonesHomeodomain ProteinsIL1B protein, mouseInterferon-gammaInterleukin-17Interleukin-1betaInterleukin-2Interleukin-23Interleukin-6Nuclear Receptor Subfamily 1, Group F, Member 1Nuclear Receptor Subfamily 1, Group F, Member 3RAG-1 proteinRNA, Small InterferingRora protein, mouseRorc protein, mouseRunx1 protein, mouseTransforming Growth Factor betaColitisRunx1TGF-βTh1Th17

Identifiers

PMID25605286
PMCPMC4441226
OpenAlexW1492966940

What OpenQuestion holds

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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.