ArticleFrontiers in immunology2023
Oncostatin M suppresses
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Mechanisms of pruritus and advances in traditional Chinese medicine therapy (Review).Molecular medicine reports · 2026Review
- Review
- The neuro-immune insights of itch: peripheral mechanisms and central glial contributions.Cellular & molecular biology letters · 2026Review
- Use of bidirectional Mendelian randomization to unveil the association between antibody-mediated immune responses to infectious agents and allergic rhinitis.Human vaccines & immunotherapeutics · 2025Review
- Oncostatin M enhances the lengthening of sensory nerves and skin hypersensitivity.Frontiers in immunology · 2025Article
- Macrophage Functions in Psoriasis: Lessons from Mouse Models.International journal of molecular sciences · 2024Review
- Article
- High-parameter immunophenotyping reveals distinct immune cell profiles in pruritic dogs and cats.Frontiers in veterinary science · 2024Article
- Exploring causal correlations between circulating cytokines and atopic dermatitis: a bidirectional two-sample Mendelian randomization study.Frontiers in immunology · 2024Article
- Abrocitinib Monotherapy for Refractory Prurigo Nodularis: Report of Two Successful Cases.Clinical, cosmetic and investigational dermatology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by intermittent itchy rash. Type 2 inflammatory cytokines such as interleukin (IL)-4, IL-13, and IL-31 are strongly implicated in AD pathogenesis. Stimulation of IL-31 cognate receptors on C-fiber nerve endings is believed to activate neurons in the dorsal root ganglion (DRG), causing itch. The IL-31 receptor is a heterodimer of OSMRβ and IL31RA subunits, and OSMRβ can also bind oncostatin M (OSM), a pro-inflammatory cytokine released by monocytes/macrophages, dendritic cells, and T lymphocytes. Further, OSM expression is enhanced in the skin lesions of AD and psoriasis vulgaris patients. Objective: The current study aimed to examine the contributions of OSM to AD pathogenesis and symptom expression. Methods: The expression levels of the OSM gene ( Results: We confirmed overexpression of Conclusion: These results suggest that OSM is an important cytokine in the regulation of skin monocytes, promoting the actions of IL-4 and IL-13 in the DRG and suppressing the action of IL-31. It is speculated that OSM released from monocytes in skin modulates the sensitivity of DRG neurons to type 2 inflammatory cytokines and thereby the severity of AD-associated skin itch.
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Registered trials
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.