Evidence map›Paper›PMID 40651664›Full record

SynthesisThe Journal of allergy and clinical immunology2025

IL31 identified as a key genetic risk factor for prurigo nodularis.

Matthew T Patrick, Yuntian Wu, Xue Zhong, Qinmengge Li, Valérie Julia, Bingshan Li, Johann E Gudjonsson, Lam C Tsoi

Abstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in The Journal of allergy and clinical immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Immunopathogenesis of itch: an integrative framework for chronic pruritus.JID innovations : skin science from molecules to population health · 2026
    Review
  2. Review
  3. Article
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

8 authors.

Matthew T PatrickDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, Mich.
Yuntian WuDepartment of Biostatistics, University of Michigan, Ann Arbor, Mich.
Xue ZhongDivision of Genetic Medicine, Department of Medicine, Vanderbilt University, Nashville, Tenn.
Qinmengge LiDepartment of Biostatistics, University of Michigan, Ann Arbor, Mich.
Valérie JuliaGalderma, Zug, Switzerland.
Bingshan LiDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tenn.
Johann E GudjonssonDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, Mich; Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, Mich.
Lam C TsoiDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, Mich; Department of Biostatistics, University of Michigan, Ann Arbor, Mich; Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, Mich; Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Mich. Electronic address: alextsoi@med.umich.edu.

Funding

Immunogenomics and Systems Biology CoreUC2AR081033 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Johann Eli Gudjonsson, Lam Cheung Tsoi · 2022 to 2026
$3.3M
Integrative and trans-ethnic study to understand psoriasis associated signalsR01AR080662 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Lam Cheung Tsoi · 2023 to 2026
$1.4M
Integrative Biology Approach to Identify and Characterize Roles of lncRNAs Associated with Psoriasis PathologyK01AR072129 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TSOI, LAM CHEUNG · 2017 to 2021
$500k
NIAMS NIH HHS K01 AR072129NIAMS NIH HHS R01 AR080662NIAMS NIH HHS UC2 AR081033
6 · The paper itself

Abstract

backgroundAlthough previous studies have suggested that genetic risk factors can contribute to the development of prurigo nodularis (PN), little is known about the specific variants involved.

objectiveWe aimed to test which genetic variants increase predisposition to PN by conducting a large genome-wide association study.

methodsFive separate cohorts (4239 case patients with PN and 583,544 controls) were combined through genome-wide association study meta-analysis, and the results were validated by using the Michigan Genomics Initiative. Data from regulatory regions and expression quantitative trait loci were applied to investigate genetic mechanisms.

resultsWe identified a genome-wide significant genetic signal for PN (P = 7.5 × 10

conclusionOur results reinforce the role of genetics in PN and advance understanding of the mechanisms and their relationship with other pruritic inflammatory skin diseases.

Indexed as

Genetic Predisposition to DiseaseInterleukinsPrurigoFemaleGenome-Wide Association StudyHumansMalePolymorphism, Single NucleotideQuantitative Trait LociRisk FactorsInterleukinscytokinesGenome-wide association studiesitchprurigo nodularis

Identifiers

PMID40651664
PMCPMC13135726

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.