Evidence map›Paper›PMID 21525389›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Stat4 is critical for the balance between Th17 cells and regulatory T cells in colitis.

Jiangnan Xu, Yu Yang, Guixing Qiu, Girdhari Lal, Na Yin, Zhihong Wu, Jonathan S Bromberg, Yaozhong Ding

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022
    Article
  8. Article
  9. Review
  10. STAT4: an immunoregulator contributing to diverse human diseases.International journal of biological sciences · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. STAT4 Regulates the CD8Journal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  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

8 authors at 3 institutions in 2 countries.

Jiangnan XuCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Yu Yang
Guixing Qiu
Girdhari Lal
Na Yin
Zhihong Wu
Jonathan S Bromberg
Yaozhong Ding
University of Maryland, Baltimore · USPeking Union Medical College Hospital · CNIcahn School of Medicine at Mount Sinai · US

Funding

Transplantation Tolerance: T Cell TraffickingR01AI041428 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROMBERG, JONATHAN S · 1997 to 2012
$3.3M
IL-6 and early Th2 commitmentR01AI062855 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI DING, YAOZHONG · 2005 to 2009
$1.6M
NIAID NIH HHS R01 AI041428NIAID NIH HHS R01 AI062855NIAID NIH HHS R01 AI 62855NIAID NIH HHS R0I AI 41428
6 · The paper itself

Abstract

Th17 play a central role in autoimmune inflammatory responses. Th1 are also necessary for autoimmune disease development. The interplay of Th1 signals and how they coordinate with Th17 during inflammatory disease pathogenesis are incompletely understood. In this study, by adding Stat4 deficiency to Stat6/T-bet double knockout, we further dissected the role of Stat4 in Th1 development and colitis induction. We showed that in the absence of the strong Th2 mediator Stat6, neither Stat4 nor T-bet is required for IFN-γ production and Th1 development. However, addition of Stat4 deficiency abolished colitis induced by Stat6/T-bet double-knockout cells, despite Th1 and Th17 responses. The failure of colitis induction by Stat4/Stat6/T-bet triple-knockout cells is largely due to elevated Foxp3(+) regulatory T cell (Treg) development. These results highlight the critical role of Stat4 Th1 signals in autoimmune responses in suppressing Foxp3(+) Treg responses and altering the balance between Th17 and Tregs to favor autoimmune disease.

Indexed as

AnimalsCD11c AntigenCD4-Positive T-LymphocytesCells, CulturedCoculture TechniquesColitisDendritic CellsForkhead Transcription FactorsImmunohistochemistryInterferon-gammaInterleukin-12Interleukin-4MiceMice, Inbred BALB CMice, KnockoutMice, SCIDCD11c AntigenForkhead Transcription FactorsFoxp3 protein, mouseInterferon-gammaInterleukin-12Interleukin-4Stat4 protein, mouseSTAT4 Transcription FactorStat6 protein, mouseSTAT6 Transcription FactorT-bet Transcription FactorT-Box Domain Proteins

Identifiers

PMID21525389
PMCPMC3098937
OpenAlexW1943072952

What OpenQuestion holds

Textmetadata
LicenceTDM
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.