Evidence map›Paper›PMID 24736726›Full record

ArticleScientific reports2014

ASK1 promotes the contact hypersensitivity response through IL-17 production.

Junya Mizukami, Takehiro Sato, Montserrat Camps, Hong Ji, Thomas Rueckle, Dominique Swinnen, Ryoji Tsuboi, Kohsuke Takeda, Hidenori Ichijo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
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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

9 authors.

Junya Mizukami1] Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan, 113-0033 [2] Department of Dermatology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo, Japan, 160-0023.
Takehiro SatoLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan, 113-0033.
Montserrat CampsDepartments of Inflammation, Merck Serono International S.A., 1202 Geneva, Switzerland.
Hong JiNovo Nordisk A/S, Novo Nordisk Park, DK-2760 Måløv, Denmark.
Thomas RueckleMedicines for Malaria Venture, Department of Translational Medicine, Route de Pré-Bois 20, CH-1215 Geneva, Switzerland.
Dominique SwinnenDepartment of Chemistry, Merck Serono International S.A., 1202 Geneva, Switzerland.
Ryoji TsuboiDepartment of Dermatology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo, Japan, 160-0023.
Kohsuke Takeda1] Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan, 113-0033 [2] Division of Cell Regulation, Graduate School of Biomedical Sciences, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan.
Hidenori IchijoLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan, 113-0033.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Contact hypersensitivity (CHS) is a form of delayed-type hypersensitivity triggered by the response to reactive haptens (sensitization) and subsequent challenge (elicitation). Here, we show that ASK1 promotes CHS and that suppression of ASK1 during the elicitation phase is sufficient to attenuate CHS. ASK1 knockout (KO) mice exhibited impaired 2,4-dinitrofluorobenzene (DNFB)-induced CHS. The suppression of ASK1 activity during the elicitation phase through a chemical genetic approach or a specific inhibitory compound significantly reduced the CHS response to a level similar to that observed in ASK1 KO mice. The reduced response was concomitant with the strong inhibition of production of IL-17, a cytokine that plays an important role in CHS and other inflammatory diseases, from sensitized lymph node cells. These results suggest that ASK1 is relevant to the overall CHS response during the elicitation phase and that ASK1 may be a promising therapeutic target for allergic contact dermatitis and other IL-17-related inflammatory diseases.

Indexed as

AnimalsCD4-Positive T-LymphocytesDermatitis, ContactDinitrofluorobenzeneDisease Models, AnimalHEK293 CellsHumansInterferon-gammaInterleukin-17MAP Kinase Kinase Kinase 5MiceMice, Inbred C57BLMice, Knockoutp38 Mitogen-Activated Protein KinasesDinitrofluorobenzeneInterferon-gammaInterleukin-17Map3k5 protein, mouseMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein Kinases

Identifiers

PMID24736726
PMCPMC3988482

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Registered trials

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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.