ArticleFrontiers in immunology2018
IL-36γ Is a Strong Inducer of IL-23 in Psoriatic Cells and Activates Angiogenesis.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Review
- Mesangial Cells (MES-SV40) Cultured in High Glucose Produce IL-36α, Which Is Associated with Type 2 Diabetes Mellitus.International journal of molecular sciences · 2026Article
- IL-37 and IL-36 Cytokine Profiles in Chronic Hepatitis Delta During Bulevirtide Therapy.Pathogens (Basel, Switzerland) · 2026Article
- Endothelial IL-36 receptor activation promotes vascular stability to limit pathological microvessel permeability in the CNS.Cell reports · 2025Article
- IL-17 Class Inhibitors and Plaque Psoriasis: Not All Biologics Relapse Equally.The Journal of clinical and aesthetic dermatology · 2025Article
- Epidermal proteomics demonstrates Elafin as a psoriasis-specific biomarker and highlights increased anti-inflammatory activity around psoriatic plaques.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Article
- Article
- Cutaneous dysbiosis characterizes the post-allogeneic hematopoietic stem cell transplantation period.Blood advances · 2025Observational
- Roles for Exosomes in the Pathogenesis, Drug Delivery and Therapy of Psoriasis.Pharmaceutics · 2025Review
- Interventions in cytokine signaling: novel horizons for psoriasis treatment.Frontiers in immunology · 2025Review
- IWR-1 attenuates the promotional effect of IL-36γ in a mouse model of psoriasis.BMC immunology · 2024Article
- Unveiling the overlooked fungi: the vital of gut fungi in inflammatory bowel disease and colorectal cancer.Gut pathogens · 2024Review
- Generalized Pustular Psoriasis and Systemic Organ Dysfunctions.International journal of molecular sciences · 2024Review
- Functional Genomics and Insights into the Pathogenesis and Treatment of Psoriasis.Biomolecules · 2024Review
- The implications of exosomes in psoriasis: disease: emerging as new diagnostic markers and therapeutic targets.Molecular biology reports · 2024Review
- Sublingual Immunotherapy Decreased the Serum Levels of Interleukin-36Mediators of inflammation · 2024Article
- Dynamics of a network mediated by IL-36 and involved in the pathogenesis of psoriasis.Frontiers in network physiology · 2024Article
- IL-36γ Augments Ocular Angiogenesis by Promoting the Vascular Endothelial Growth Factor-Vascular Endothelial Growth Factor Receptor Axis.The American journal of pathology · 2023Article
- Increased Interleukin-36β Expression Promotes Angiogenesis in Japanese Atopic Dermatitis.International journal of molecular sciences · 2023Article
- Increased expression of ELOVL7 contributes to production of inflammatory cytokines in THP-1 cell-derived M1-like macrophages.Journal of clinical biochemistry and nutrition · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The IL-1 family member cytokine IL-36γ is recognised as key mediator in the immunopathology of psoriasis, hallmarks of which involve the activation of both resident and infiltrating inflammatory myeloid cells and aberrant angiogenesis. This research demonstrates a role for IL-36γ in both myeloid activation and angiogenesis. We show that IL-36γ induces the production of psoriasis-associated cytokines from macrophages (IL-23 and TNFα) and that this response is enhanced in macrophages from psoriasis patients. This effect is specific for IL-36γ and could not be mimicked by other IL-1 family cytokines such as IL-1α. IL-36γ was also demonstrated to induce endothelial tube formation and branching, in a VEGF-A-dependent manner. Furthermore, IL-36γ-stimulated macrophages potently activated endothelial cells and led to increased adherence of monocytes, effects that were markedly more pronounced for psoriatic macrophages. Interestingly, regardless of stimulus, psoriasis monocytes showed increased adherence to both the stimulated and unstimulated endothelium when compared with monocytes from healthy individuals. Collectively, these findings show that IL-36γ has the potential to enhance endothelium directed leucocyte infiltration into the skin and strengthen the IL-23/IL-17 pathway adding to the growing evidence of pathogenetic roles for IL-36γ in psoriatic responses. Our findings also point to a cellular response, which could potentially explain cardiovascular comorbidities in psoriasis in the form of endothelial activation and increased monocyte adherence.
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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.