Evidence map›Paper›PMID 17951529›Full record

ArticleBlood2008

Retinoic acid inhibits Th17 polarization and enhances FoxP3 expression through a Stat-3/Stat-5 independent signaling pathway.

Kevin M Elias, Arian Laurence, Todd S Davidson, Geoffrey Stephens, Yuka Kanno, Ethan M Shevach, John J O'Shea

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
228citing papers in PubMed, 1 pooled it
14.0field-weighted citation impact, top 1% 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

228 citing papers in PubMed, 1 synthesis or guideline pooled it, 442 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Review
  7. Article
  8. [Research Progress of Peripheral Immune Tolerance in Oral Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025
    Review
  15. The gut microbiome connects nutrition and human health.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  16. Vitamin A and Its Related Diseases.Food science & nutrition · 2025
    Review
  17. Article
  18. Article
  19. Review
  20. Article

168 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Kevin M EliasHoward Hughes Medical Institute National Institutes of Health Research Scholars Program, Bethesda, MD, USA.
Arian Laurence
Todd S Davidson
Geoffrey Stephens
Yuka Kanno
Ethan M Shevach
John J O'Shea
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USNational Institute of Allergy and Infectious Diseases · US

Funding

Stat transcription factors in immunoregulation and autoimmune diseaseZIAAR041159 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN · 2009 to 2025
$49.3M
Studies of the Function of Naturally Occurring and Adaptive T Regulatory CellsZIAAI000959 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHEVACH, ETHAN · 2009 to 2025
$17.6M
Studies of the Function of Naturally Occurring and Adaptive T Regulatory CellsZ01AI000959 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHEVACH, ETHAN M. · 2006 to 2008
$5.1M
Stat transcription factors in immunoregulation and autoimmune diseaseZ01AR041159 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN · 2008 to 2008
$1.8M
6 · The paper itself

Abstract

CD4(+) helper T (Th) cells play a crucial role in the delicate balance between host defense and autoimmune disease. Two important populations of helper T cells are the proinflammatory, interleukin-17 (IL-17)-producing (Th17) cells and the anti-inflammatory forkhead box P3-positive (FoxP3(+)) T regulatory (Treg) cells. Here we show that all-trans retinoic acid (ATRA) and other agonists of the retinoic acid receptor alpha (RARalpha) inhibit the formation of Th17 cells and promote FoxP3 expression. Conversely, inhibition of retinoic acid signaling constrains transforming growth factor beta (TGF-beta1) induction of FoxP3. The effect of ATRA is mediated independently of IL-2, signal transducer and activator of transcription 5 (Stat5) and Stat3, representing a novel mechanism for the induction of FoxP3 in CD4 T cells. As previous studies have shown that vitamin A derivatives are protective in animal models of autoimmune disease, the current data suggest a previously unrecognized role for RARalpha in the regulation of CD4(+) T-cell differentiation and provide a mechanism for the anti-inflammatory effects of retinoic acid.

Indexed as

AnimalsCell DedifferentiationCells, CulturedForkhead Transcription FactorsInterleukin-17Interleukin-2MiceMice, Inbred C57BLReceptors, Retinoic AcidRetinoic Acid Receptor alphaSignal TransductionSTAT3 Transcription FactorSTAT5 Transcription FactorT-Lymphocytes, Helper-InducerTretinoinForkhead Transcription FactorsFoxp3 protein, mouseInterleukin-17Interleukin-2Rara protein, mouseReceptors, Retinoic AcidRetinoic Acid Receptor alphaSTAT3 Transcription FactorSTAT5 Transcription FactorTretinoin

Identifiers

PMID17951529
PMCPMC2214761
OpenAlexW2160836190

What OpenQuestion holds

Textmetadata
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.