ReviewInternational journal of molecular sciences2019
The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 139 citations in OpenAlex.
- Cutaneous Manifestations in Psoriatic Arthritis: Phenotypes, Clinical Burden, and Therapeutic Implications.Rheumatology and therapy · 2026Review
- IL-36-Driven Inflammation in Generalized Pustular Psoriasis: Immunological Insights from Plaque Psoriasis and Implications for Targeted Therapy.International journal of molecular sciences · 2026Review
- Review
- IL-37 and IL-36 Cytokine Profiles in Chronic Hepatitis Delta During Bulevirtide Therapy.Pathogens (Basel, Switzerland) · 2026Article
- Mast Cells Accumulate in the Stroma of Breast Adenocarcinoma and Secrete Pro-Inflammatory Cytokines and Tumor-Damaging Mediators: Could IL-37 and IL-38 Play an Anti-Tumor Role?International journal of molecular sciences · 2026Review
- Psoriasis as a spatial immune ecosystem: insights from single-cell and spatial transcriptomics.Frontiers in immunology · 2026Review
- Targeting the IL-36 Pathway: Spesolimab as a Therapeutic for Acute Flares of Pustular Psoriasis.Cureus · 2026Article
- The IL-36 Cytokine Rheostat: Hierarchical Regulation of Epithelial-Immune Crosstalk and Precision Therapy in Psoriatic and Related Dermatoses.Clinical, cosmetic and investigational dermatology · 2026Review
- A Multicenter Validation of a Fully Automated Chemiluminescence Immunoassay for Plasma Elafin in Psoriasis Diagnosis and Severity Assessment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Characteristics of peripheral blood lymphocyte subsets in elderly patients with psoriasis.Immunity & ageing : I & A · 2025Article
- Effects of combined treatment withFood science and biotechnology · 2025Article
- Emerging cytokines contribute to the clinical manifestation of carotid artery plaque formation and stability in patients with diabetes.Atherosclerosis plus · 2025Article
- Sinhyotaklisan as a Potential Therapeutic for Psoriasis: Network Pharmacology and Experimental Validation.International journal of molecular sciences · 2025Article
- Emerging Therapies for Palmoplantar Pustulosis with a Focus on IL-23 Inhibitors.Journal of clinical medicine · 2025Review
- Quantum molecular resonance ameliorates atopic dermatitis through suppression of IL36G and SPRR2B.BMB reports · 2025Article
- A Snapshot of Biomarkers in Psoriasis.Current drug discovery technologies · 2025Review
- Pharmacological Management of Psoriasis: Current Landscape and Future Perspectives.Recent advances in inflammation & allergy drug discovery · 2025Review
- Biologics and small molecules for psoriasis: current and future progress.Drugs in context · 2025Review
- Skin immunity and inflammation: cellular interactions and communication.Clinical & translational immunology · 2025Review
- Dichotomous roles of IL-36 and IL-38 in cardiovascular disease.Frontiers in immunology · 2025Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Psoriasis is an immune-mediated inflammatory skin disease that involves mainly T helper (Th)17, Th1 and Th22 lymphocytes, which cause hyper-proliferation of the epidermis with aberrant differentiation of keratinocytes, and local production of chemokines and cytokines. These fuel a self-amplifying loop where these products act on T cells to perpetuate cutaneous inflammatory processes. Among the various inflammatory mediators involved, interleukin (IL)-36 cytokines are important for the recruitment and activation of neutrophils and Th17 cells in psoriatic skin. In particular, IL-36s induce chemokines and cytokines interfere with differentiation/cornification programs in the epidermis, as well as promote pathological angiogenesis and endothelial cell activation. IL-36 cytokines belong to the IL-1 family, and comprise IL-36α, IL-36β, and IL-36γ agonists as well as IL-36 receptor antagonist and IL-38 antagonists. IL-36 cytokines are up-regulated in psoriatic epidermis, and their expression is strongly induced by TNF-α and IL-17. Contrarily, IL-38 antagonist is downregulated, and its impaired expression may be relevant to the dysregulated inflammatory processes induced by IL-36. Here, we discuss on the pathogenic mechanisms leading to the altered balance of IL-36 agonists/antagonists and the significance of this dysregulation in psoriasis. Collection of the information will provide a theoretical basis for the development of novel therapeutic strategies based on IL-36 agonist/antagonist manipulation in psoriasis.
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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.