Evidence map›Paper›PMID 15667561›Full record

ArticleImmunology2005

Interleukin-24 and its receptors.

Mai Wang, Peng Liang

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

43 citing papers in PubMed, 100 citations in OpenAlex.

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  11. Interleukin-22 receptor 1-mediated stimulation of T-type CaCell communication and signaling : CCS · 2024
    Article
  12. Immune Mechanisms of Pulmonary Fibrosis with Bleomycin.International journal of molecular sciences · 2023
    Review
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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 1 institution in 1 country.

Mai WangDepartment of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Peng Liang
Vanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 24 (IL-24) is a new member of the IL-10 family of cytokines and it signals through two heterodimeric receptors: IL-20R1/IL-20R2 and IL-22R1/IL-20R2. Upon binding to its receptors, IL-24 induces rapid activation of Stat-1 and Stat-3 transcription factors, which appear to play a role in cell survival and proliferation. Under physiological conditions, the major sources of IL-24 are the activated monocytes and T helper 2 cells, whereas the major IL-24 target tissues, based on the receptor expression pattern, are non-haematopoietic in origin, and include skin, lung and reproductive tissues. Structurally and functionally, IL-24 is highly conserved across species. This review highlights our current knowledge of IL-24 as a cytokine, with much less emphasis placed on the non-receptor-mediated functions (a subject of several reviews) focused on in much of the earlier literature on IL-24. The potential roles of IL-24 as part of a complex cytokine network in wound healing, psoriasis and cancer are discussed.

Indexed as

Signal TransductionCell ProliferationGenes, Tumor SuppressorHumansInterleukin-24InterleukinsLymphocytesNeoplasmsPsoriasisReceptors, InterleukinWound Healinginterleukin-20 receptorInterleukin-24InterleukinsReceptors, Interleukin

Identifiers

PMID15667561
PMCPMC1782067
OpenAlexW2066952519

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.