Evidence map›Paper›PMID 19290934›Full record

ReviewImmunological reviews2009

Janus kinases in immune cell signaling.

Kamran Ghoreschi, Arian Laurence, John J O'Shea

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Immunological reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 511 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
511citing papers in PubMed, 7 pooled it
22.7field-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

511 citing papers in PubMed, 7 syntheses or guidelines pooled it, 1,132 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Janus kinase inhibitors for the treatment of COVID-19.The Cochrane database of systematic reviews · 2022
    Pooled it
  6. Guideline
  7. Pooled it
  8. Trial
  9. Trial
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. The Role of TYK2 Inhibitors in the Pathogenesis and Treatment of Psoriasis.The Journal of clinical and aesthetic dermatology · 2026
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

451 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

3 authors at 1 institution in 1 country.

Kamran GhoreschiMolecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA. ghoreschik@mail.nih.gov
Arian Laurence
John J O'Shea
National Institutes of Health · 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
Targeting Janus kinases in the treatment of autoimmune diseaseZIAAR041106 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN · 2009 to 2024
$4.8M
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
Cytokine Signaling and Primary ImmunodeficiencyZIAAR041167 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN · 2009 to 2019
$2.3M
Intramural NIH HHS Z01 AR041106
6 · The paper itself

Abstract

The Janus family kinases (Jaks), Jak1, Jak2, Jak3, and Tyk2, form one subgroup of the non-receptor protein tyrosine kinases. They are involved in cell growth, survival, development, and differentiation of a variety of cells but are critically important for immune cells and hematopoietic cells. Data from experimental mice and clinical observations have unraveled multiple signaling events mediated by Jaks in innate and adaptive immunity. Deficiency of Jak3 or Tyk2 results in defined clinical disorders, which are also evident in mouse models. A striking phenotype associated with inactivating Jak3 mutations is severe combined immunodeficiency syndrome, whereas mutation of Tyk2 results in another primary immunodeficiency termed autosomal recessive hyperimmunoglobulin E syndrome. By contrast, complete deletion of Jak1 or Jak2 in the mouse are not compatible with life and, unsurprisingly, do not have counterparts in human disease. However, activating mutations of each of the Jaks are found in association with malignant transformation, the most common being gain-of-function mutations of Jak2 in polycythemia vera and other myeloproliferative disorders. Our existing knowledge on Jak signaling pathways and fundamental work on their biochemical structure and intracellular interactions allow us to develop new strategies for controlling autoimmune diseases or malignancies by developing selective Jak inhibitors, which are now coming into clinical use. Despite the fact that Jaks were discovered only a little more than a decade ago, at the time of writing there are 20 clinical trials underway testing the safety and efficacy of Jak inhibitors.

Indexed as

Signal TransductionAnimalsHumansJanus KinasesMyeloproliferative DisordersSevere Combined ImmunodeficiencyJanus Kinases

Identifiers

PMID19290934
PMCPMC2782696
OpenAlexW2151734278

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.