Evidence map›Paper›PMID 34857395›Full record

ArticleThe Journal of allergy and clinical immunology2022

Transcriptomic characterization of prurigo nodularis and the therapeutic response to nemolizumab.

Lam C Tsoi, Feriel Hacini-Rachinel, Paul Fogel, Francois Rousseau, Xianying Xing, Matthew T Patrick, Allison C Billi, Celine C Berthier, J Michelle Kahlenberg, Anne Lazzari and 6 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of allergy and clinical immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
11.3field-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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 89 citations in OpenAlex.

  1. IL31 identified as a key genetic risk factor for prurigo nodularis.The Journal of allergy and clinical immunology · 2025
    Pooled it
  2. Pooled it
  3. Nemolizumab in prurigo nodularis up to 100 weeks: OLYMPIA LTE interim analysis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Trial
  4. Trial
  5. Immunopathogenesis of itch: an integrative framework for chronic pruritus.JID innovations : skin science from molecules to population health · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Th2 mRNA gene expression analysis separates Prurigo nodularis into two immune signature groups.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025
    Observational
  16. Article
  17. Host-Microbiome Interactions in Chronic Itch.Journal of clinical medicine · 2025
    Review
  18. Article
  19. Type 2 Inflammation and Its Role in Dermatologic Diseases.International journal of dermatology · 2025
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 3 countries.

Lam C TsoiDepartment of Dermatology, University of Michigan, Ann Arbor, Mich; Department of Biostatistics, University of Michigan, Ann Arbor, Mich; Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Mich.
Feriel Hacini-RachinelGalderma, La Tour-De-Peilz, Switzerland.
Paul FogelGalderma, La Tour-De-Peilz, Switzerland.
Francois RousseauGalderma, La Tour-De-Peilz, Switzerland.
Xianying XingDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
Matthew T PatrickDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
Allison C BilliDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
Celine C BerthierDepartment of Internal Medicine, Division of Nephrology, University of Michigan, Ann Arbor, Mich.
J Michelle KahlenbergDepartment of Internal Medicine, Division of Rheumatology, University of Michigan, Ann Arbor, Mich; Taubman Medical Research Institute, University of Michigan Medical School, Ann Arbor, Mich.
Anne LazzariGalderma, La Tour-De-Peilz, Switzerland.
Henning WiegmannDepartment of Dermatology and Center for Chronic Pruritus, University Hospital Münster, Münster, Germany.
Sonja StänderDepartment of Dermatology and Center for Chronic Pruritus, University Hospital Münster, Münster, Germany.
Christophe PikettyGalderma, La Tour-De-Peilz, Switzerland.
Valerie JuliaGalderma, La Tour-De-Peilz, Switzerland.
Jayendra Kumar KrishnaswamyGalderma, La Tour-De-Peilz, Switzerland.
Johann E GudjonssonDepartment of Dermatology, University of Michigan, Ann Arbor, Mich; Taubman Medical Research Institute, University of Michigan Medical School, Ann Arbor, Mich. Electronic address: johanng@umich.edu.
Galderma (Switzerland) · CHUniversity of Michigan–Ann Arbor · USA. Alfred Taubman Health Care Center · USUniversity Hospital Münster · DE

Funding

University of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PENNATHUR, SUBRAMANIAM · 2008 to 2022
$12.9M
University of Michigan Skin Biology and Diseases Resource-based CenterP30AR075043 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Johann Eli Gudjonsson · 2019 to 2026
$6.6M
Kallikrein-PAR interactions in skin inflammationR01AR073196 · NIAMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WARD, NICOLE LEANNE · 2018 to 2023
$3.3M
Role of IL-13 and the IL-13 Associated rs20541 Risk Variant in the Pathogenesis of PsoriasisR01AR069071 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUDJONSSON, JOHANN ELI · 2015 to 2019
$2.1M
Mechanisms of sex discrepancy in autoimmune disease: Regulation of the female-biased VGLL3 immune pathwayK08AR078251 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BILLI, ALLISON CHELSA · 2021 to 2025
$865k
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 K08 AR078251NIAMS NIH HHS P30 AR075043NIAMS NIH HHS R01 AR069071NIAMS NIH HHS R01 AR073196NIDDK NIH HHS P30 DK081943
6 · The paper itself

Abstract

backgroundPrurigo nodularis (PN) is a debilitating, difficult-to-treat, intensely pruritic, chronic inflammatory skin disease characterized by hyperkeratotic skin nodules. The pathogenesis of PN is not well understood but is believed to involve cross talk between sensory nerve fibers, immune cells, and the epidermis. It is centered around the neuroimmune cytokine IL-31, driving an intractable itch-scratch cycle.

objectiveWe sought to provide a comprehensive view of the transcriptomic changes in PN skin and characterize the mechanism of action of the anti-IL-31 receptor inhibitor nemolizumab.

methodRNA sequencing of biopsy samples obtained from a cohort of patients treated with the anti-IL-31 receptor inhibitor nemolizumab and taken at baseline and week 12. Generation and integration of patient data with RNA-Seq data generated from reconstructed human epidermis stimulated with IL-31 and other proinflammatory cytokines.

resultsOur results demonstrate that nemolizumab effectively decreases IL-31 responses in PN skin, leading to effective suppression of downstream inflammatory responses including T

conclusionThese data demonstrate a broad response to IL-31 receptor inhibition with nemolizumab and confirm the critical upstream role of IL-31 in PN pathogenesis.

Indexed as

PrurigoAntibodies, Monoclonal, HumanizedChronic DiseaseCytokinesHumansPruritusTranscriptomeAntibodies, Monoclonal, HumanizedCytokinesnemolizumabmechanismnemolizumabPrurigo nodularisT(H)17T(H)2

Identifiers

PMID34857395
PMCPMC8995330
OpenAlexW3216784684

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.