ArticleNeuroscience bulletin2018
TNF-α/TNFR1 Signaling is Required for the Full Expression of Acute and Chronic Itch in Mice via Peripheral and Central Mechanisms.
Article in Neuroscience bulletin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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.
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.
Who cites it
27 citing papers in PubMed, 60 citations in OpenAlex.
- Cutaneous plasmacytosis with atypical clinical behavior in two dogs.The Journal of veterinary medical science · 2026Article
- Astrocyte-Specific Upregulation of Tumor Necrosis Factor Receptor II Ameliorates Pathological Phenotypes in APPNeuroscience bulletin · 2026Article
- Psilocin alleviates acute itch in mice: possible involvement of 5-HT2A receptors and kynurenine pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- An injectable and biodegradable zwitterionic gel for extending the longevity and performance of insulin infusion catheters.Nature biomedical engineering · 2024Article
- Mechanism of pruritus ani lotion combined with Huajiao-Gancao-Bingpian oil for pruritus ani treatment based on network pharmacology and molecular dynamics.Postepy dermatologii i alergologii · 2024Article
- Dendritic cells under allergic condition enhance the activation of pruritogen-responsive neurons via inducing itch receptors in a co-culture study.BMC immunology · 2024Article
- Regulatory Mechanism of the IL-33-IL-37 Axis via Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis.International journal of molecular sciences · 2023Review
- Pruritogenic molecules in the skin of patients with dermatomyositis.Frontiers in medicine · 2023Article
- Review
- Itch in Hymenoptera Sting Reactions.Frontiers in allergy · 2021Article
- Formalin Itch Test: Low-Dose Formalin Induces Histamine-Independent, TRPA1-Mediated Itch in Mice.Frontiers in medicine · 2021Article
- The Role of Transient Receptor Potential A1 and G Protein-Coupled Receptor 39 in Zinc-Mediated Acute and Chronic Itch in Mice.Frontiers in molecular neuroscience · 2021Article
- Physiology and Pathophysiology of Itch.Physiological reviews · 2020Review
- Spinal cord NLRP1 inflammasome contributes to dry skin induced chronic itch in mice.Journal of neuroinflammation · 2020Article
- Mechanisms and Management of Itch in Dry Skin.Acta dermato-venereologica · 2020Review
- More than Scratching the Surface: Recent Progress in Brain Mechanisms Underlying Itch and Scratch.Neuroscience bulletin · 2020Review
- Astrocytes in chronic pain and itch.Nature reviews. Neuroscience · 2019Review
- Expression of tumor necrosis factor receptor 2 in human non-small cell lung cancer and its role as a potential prognostic biomarker.Thoracic cancer · 2019Article
- Qingpeng Ointment Ameliorates Inflammatory Responses and Dysregulation of Itch-Related Molecules for Its Antipruritic Effects in Experimental Allergic Contact Dermatitis.Frontiers in pharmacology · 2019Article
- Relationship between the Degrees of Itch and Serum Lipocalin-2 Levels in Patients with Psoriasis.Journal of immunology research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that cytokines and chemokines play crucial roles in chronic itch. In the present study, we evaluated the roles of tumor necrosis factor-alpha (TNF-α) and its receptors TNF receptor subtype-1 (TNFR1) and TNFR2 in acute and chronic itch in mice. Compared to wild-type (WT) mice, TNFR1-knockout (TNFR1-KO) and TNFR1/R2 double-KO (DKO), but not TNFR2-KO mice, exhibited reduced acute itch induced by compound 48/80 and chloroquine (CQ). Application of the TNF-synthesis inhibitor thalidomide and the TNF-α antagonist etanercept dose-dependently suppressed acute itch. Intradermal injection of TNF-α was not sufficient to evoke scratching, but potentiated itch induced by compound 48/80, but not CQ. In addition, compound 48/80 induced TNF-α mRNA expression in the skin, while CQ induced its expression in the dorsal root ganglia (DRG) and spinal cord. Furthermore, chronic itch induced by dry skin was reduced by administration of thalidomide and etanercept and in TNFR1/R2 DKO mice. Dry skin induced TNF-α expression in the skin, DRG, and spinal cord and TNFR1 expression only in the spinal cord. Thus, our findings suggest that TNF-α/TNFR1 signaling is required for the full expression of acute and chronic itch via peripheral and central mechanisms, and targeting TNFR1 may be beneficial for chronic itch treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.