Evidence map›Paper›PMID 34757808›Full record

ArticleScience translational medicine2021

Oncostatin M can sensitize sensory neurons in inflammatory pruritus.

Pang-Yen Tseng, Mark A Hoon

Open access · greenAbstract read
In one paragraph

Article in Science translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
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

61 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Immunopathogenesis of itch: an integrative framework for chronic pruritus.JID innovations : skin science from molecules to population health · 2026
    Review
  3. Article
  4. Article
  5. The mask slipped: wakeable nociceptors express OSMR/SST.Pflugers Archiv : European journal of physiology · 2026
    Article
  6. Neural cell state modulation bybioRxiv : the preprint server for biology · 2026
    Article
  7. Review
  8. Article
  9. Review
  10. Basophils activate oncostatin M receptor-expressing vagal sensory neurons.The Journal of allergy and clinical immunology · 2026
    Article
  11. Review
  12. Review
  13. Clinical Profile of Elderly Atopic Dermatitis in China.Clinical, cosmetic and investigational dermatology · 2026
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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
  20. Article

1 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

2 authors at 1 institution in 1 country.

Pang-Yen TsengMolecular Genetics Section, National Institute of Dental and Craniofacial Research/NIH, 35 Convent Drive, Bethesda, MD 20892, USA.ORCID 0000-0003-2039-0002
Mark A HoonMolecular Genetics Section, National Institute of Dental and Craniofacial Research/NIH, 35 Convent Drive, Bethesda, MD 20892, USA.ORCID 0000-0002-8794-1684
National Institute of Dental and Craniofacial Research · US

Funding

Molecular Genetic Studies of SomatosensationZIADE000721 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI HOON, MARK · 2009 to 2025
$26.6M
Intramural NIH HHS ZIA DE000721
6 · The paper itself

Abstract

Chronic itch is a major symptom of many inflammatory skin diseases. This type of pruritus is thought to be facilitated by cytokines that activate cutaneous nerve fibers; however, the molecular components and mechanisms involved are poorly understood. We found that the cytokine oncostatin M (OSM) is highly up-regulated in psoriasis, atopic dermatitis, and cutaneous T cell lymphoma, diseases associated with chronic itch. OSM receptor (OSMR) is expressed by itch-selective natriuretic polypeptide B (Nppb) neurons, and single-cell sequencing showed that OSM is mainly produced by dermal T cells and monocytes. Unlike canonical pruritogens, OSM does not activate sensory neurons. Instead, it sensitizes neurons by potentiating neural responses to pruritogens and by enhancing neural excitability. Knockout of OSMR in sensory neurons attenuated OSM-sensitized itch and inflammatory itch in mice, and pharmacological antagonism of the OSMR complex effectively alleviated pruritus in experimental inflammatory dermatitis in a rodent model. Together, our results uncover OSM as an itch neuromodulator and reveal OSM signal transduction as a potential target for antipruritic therapy.

Indexed as

PruritusSensory Receptor CellsAnimalsGene Knockout TechniquesMiceMice, KnockoutOncostatin MOncostatin M Receptor beta SubunitSignal TransductionSkinOncostatin MOncostatin M Receptor beta SubunitOsmr protein, mouse

Identifiers

PMID34757808
PMCPMC9595590
OpenAlexW3212704133

What Socratic 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 Socratic graph.