ReviewInternational journal of molecular sciences2025
IL-31/33 Axis in Atopic Dermatitis.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.Clinical reviews in allergy & immunology · 2026Review
- Atopic Dermatitis Beyond the Skin Barrier: Precision Medicine Approaches to Immunological Profiling and Therapeutic Innovation.International journal of molecular sciences · 2026Review
- Single-cell transcriptomic analysis identifies a MIF-driven keratinocyte-macrophage-Th2 axis as a key inflammatory circuit in atopic dermatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Real-World Effectiveness and Safety of Upadacitinib Versus Abrocitinib in Moderate-to-Severe Atopic Dermatitis: A Retrospective Cohort Study.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Aeroallergens in Atopic Dermatitis and Chronic Urticaria.Current allergy and asthma reports · 2026Review
- Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Thermosensitive Hydrogel Enables Noninvasive Extracellular Vesicle Therapy for Atopic Dermatitis.Biomaterials research · 2026Article
- Microbiota-directed therapies for atopic dermatitis: a three-tier framework for inflammation control, immune modulation, and microbiome restoration.Frontiers in immunology · 2026Review
- A descriptive multilevel analysis associating COVID-19 with polymyositis: from genetic markers and candidate mediators to clinical hematological profiles.Frontiers in medicine · 2026Article
- Alopecia Areata and Atopic Dermatitis: Common Mechanisms and Emerging Therapeutics.Journal of inflammation research · 2026Review
- Dupilumab-Induced Immune Drift Phenomena in Atopic Dermatitis: Novel Insights into Mechanisms and Therapeutic Strategies.Journal of clinical practice and research · 2025Review
- The Neuroimmune Axis in Atopic Dermatitis: From Pathogenic Mechanisms to Targeted Neuroimmunotherapy.Journal of inflammation research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by impaired epidermal barrier function, immune dysregulation (e.g., Th2 polarization), genetic factors (e.g., filaggrin mutations), environmental triggers and microbial dysbiosis, leading to pruritus and eczematous lesions. In this review, we present the synergistic "IL-31/IL-33 axis." IL-33, released by damaged keratinocytes, acts as an alarmin, initiating inflammation via ST2 receptors and promoting Th2 cytokine production (IL-4, IL-5, IL-13). This upregulates IL-31, primarily from Th2 cells, which directly activates sensory neurons to induce pruritus and impairs keratinocyte differentiation. Together, IL-31 and IL-33 exacerbate the itch-scratch feedback loop, barrier disruption, and inflammation. Elevated levels of IL-31 and IL-33 correlate with disease severity. Targeting the IL-31/IL-33 axis represents an emerging therapeutic option, e.g., nemolizumab (anti-IL-31RA) significantly reduces pruritus and AD symptoms in clinical trials. However, anti-IL-33/ST2 agents (e.g., etokimab, tozorakimab) demonstrate variable efficacy, highlighting complexity in targeting IL-33. Future research should prioritize biomarker-driven patient stratification to optimize the clinical application of these novel antibody-based therapies.
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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 Socratic graph.