Evidence map›Paper›PMID 17884812›Full record

ArticleThe Journal of biological chemistry2007

IL-21 is produced by Th17 cells and drives IL-17 production in a STAT3-dependent manner.

Lai Wei, Arian Laurence, Kevin M Elias, John J O'Shea

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 329 papers.

0numbers the graph read from it
0cells of the map it votes in
329citing papers in PubMed
16.3field-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

329 citing papers in PubMed, 628 citations in OpenAlex.

  1. Article
  2. Shared Pathways between Psoriasis and Atopic Dermatitis.Dermatology practical & conceptual · 2026
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  5. CD4European journal of immunology · 2026
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  8. How Cytokines Regulate Immune Response Toward Chronic Allograft Rejection?Results and problems in cell differentiation · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025
    Review
  14. Article
  15. Frontiers in immunology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024
    Review

269 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

4 authors at 3 institutions in 1 country.

Lai WeiMolecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. weil2@mail.nih.gov
Arian Laurence
Kevin M Elias
John J O'Shea
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USHoward Hughes Medical Institute · USNational Institutes of Health · US

Funding

Targeting Jak3 in the treatment of autoimmune diseaseZ01AR041106 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN J. · 1995 to 2008
$2.7M
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
Intramural NIH HHS Z01 AR041106
6 · The paper itself

Abstract

CD4(+) helper T cells can differentiate into several possible fates including: Th1, Th2, T regulatory, and Th17 cells. Although, cytokine production by non-T cells is an important factor in helper T cell differentiation, a characteristic feature of both Th1 and Th2 lineages is their ability to secrete cytokines that promote their respective differentiation. However, cytokines produced by T cells that help to sustain Th17 cells have not yet been identified. Here we show that IL-21 is a product of Th17 cells, which is induced in a Stat3-dependent manner. Additionally, Stat3 can directly bind the Il21 promoter. IL-21 also induces IL-17 production and expression of the transcription factor, RORgammat. Furthermore, generation of Th17 cells in the conventional manner is attenuated by blocking IL-21. IL-21 is known to activate Stat3 and its ability to induce Th17 differentiation is abrogated in the absence of Stat3. These data argue that IL-21 serves as an autocrine factor secreted by Th17 cells that promotes or sustains Th17 lineage commitment.

Indexed as

Gene Expression RegulationAnimalsCD4-Positive T-LymphocytesCell DifferentiationCell LineageCytokinesInterleukin-17Interleukin-21InterleukinsMiceMice, Inbred C57BLNuclear Receptor Subfamily 1, Group F, Member 3Oligonucleotide Array Sequence AnalysisPromoter Regions, GeneticReceptors, Retinoic AcidReceptors, Thyroid HormoneCytokinesInterleukin-17Interleukin-21InterleukinsNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Retinoic AcidReceptors, Thyroid HormoneRORC protein, humanRorc protein, mouseSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID17884812
PMCPMC2323680
OpenAlexW1974259787

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.