Evidence map›Paper›PMID 18172584›Full record

ReviewImmunologic research2008

Th17 cells: a new fate for differentiating helper T cells.

Zhi Chen, John J O'Shea

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
12.8field-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

124 citing papers in PubMed, 299 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. FOXP3+ T Cells-An Emerging Evidence in Periodontitis Therapeutics.Clinical and experimental dental research · 2025
    Review
  6. Frontiers in microbiology · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Relationships of circulating CD4Frontiers in immunology · 2022
    Article
  13. Article
  14. The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021
    Review
  15. Article
  16. Review
  17. Effects of aspirin, vitamin D3, and progesterone on pregnancy outcomes in an autoimmune recurrent spontaneous abortion model.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
  18. Article
  19. Article
  20. Observational

64 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

2 authors at 2 institutions in 2 countries.

Zhi ChenMolecular Immunology and Inflammation Branch, National Institutes of Arthritis, Musculoskeletal and Skin Diseases, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. zchen@utu.fi
John J O'Shea
National Institutes of Health · USUniversity of Turku · FI

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
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

Classically naïve CD4(+) have been thought to differentiate into two possible lineages, T helper 1 (Th1) or T helper 2 (Th2) cells. Within this paradigm the pathogenesis of autoimmunity was suggested to predominantly relate to Th1 cells and the production of IFN-gamma. However, there were many aspects of this model that did not seem to fit, not the least of which was that IFN-gamma was protective in some models of autoimmunity. During the past 2 years, remarkable progress has been made to characterize a new lineage of helper T cells. Designated Th17 cells, this lineage selectively produces proinflammatory cytokines including IL-17, IL-21, and IL-22. In the mouse, the differentiation of this new lineage is initiated by TGFbeta-1 and IL-6 and IL-21, which activate Stat3 and induce the expression of the transcription factor retinoic acid-related orphan receptor (RORgammat). IL-23, which also activates Stat3, apparently serves to maintain Th17 cells in vivo. In human cells, IL-1, IL-6, and IL-23 promote human Th17 differentiation, but TGFbeta-1 is reportedly not needed. Emerging data have suggested that Th17 plays an essential role in the host defense against extracellular bacteria and fungi and in pathogenesis of autoimmune diseases. Selectively targeting the Th17 lineage may be beneficial for the treatment of inflammatory and autoimmune diseases.

Indexed as

AnimalsAutoimmunityBacterial InfectionsCell DifferentiationHumansInterferon-gammaInterleukin-17Interleukin-21Interleukin-22Interleukin-6InterleukinsSTAT3 Transcription FactorT-Lymphocytes, Helper-InducerT-Lymphocytes, RegulatoryTransforming Growth Factor betaInterferon-gammaInterleukin-17Interleukin-21Interleukin-22Interleukin-6InterleukinsSTAT3 Transcription FactorTransforming Growth Factor beta

Identifiers

PMID18172584
OpenAlexW1988318286

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.