ArticleBMC medical genetics2019
Polymorphisms in IL36G gene are associated with plaque psoriasis.
Article in BMC medical genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04212507 (The Gut-Skin Axis Integrity in Psoriatic Patients), which is not on this map. Cited by 17 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.
The Gut-Skin Axis Integrity in Psoriatic Patients
Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.Immunogenetics · 2026Article
- Associations of plasma proteomic and polygenic profiling with incident psoriasis risk: a prospective cohort study.Journal of global health · 2026Article
- M2 macrophage infiltration drives tumor progression and identifies a multigene prognostic signature in esophageal cancer.Frontiers in immunology · 2025Article
- Plasma proteomics-based risk scores for psoriasis prediction: a novel approach to early diagnosis.Frontiers in immunology · 2025Article
- Psoriasis: Immunological and genetic blueprints driving pathogenesis and potential for personalized therapies.Iranian journal of basic medical sciences · 2025Review
- Signaling pathways and targeted therapies for psoriasis.Signal transduction and targeted therapy · 2023Review
- Multi-Omics Research Strategies for Psoriasis and Atopic Dermatitis.International journal of molecular sciences · 2023Review
- Proprotein convertase subtilisin/kexin type 9 is a psoriasis-susceptibility locus that is negatively related to IL36G.JCI insight · 2022Article
- L36G is associated with cutaneous antiviral competence in psoriasis.Frontiers in immunology · 2022Article
- Mechanisms and inhibitors of ferroptosis in psoriasis.Frontiers in molecular biosciences · 2022Review
- Article
- IkBζ is a Key Regulator of Tumour Necrosis Factor-a and Interleukin-17A-mediated Induction of Interleukin-36g in Human Keratinocytes.Acta dermato-venereologica · 2021Article
- "Autoinflammatory psoriasis"-genetics and biology of pustular psoriasis.Cellular & molecular immunology · 2021Review
- Variation at ACOT12 and CT62 locus represents susceptibility to psoriasis in Han population.Molecular genetics & genomic medicine · 2020Article
- The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis.International journal of molecular sciences · 2019Review
- Article
- Function and Regulation of IL-36 Signaling in Inflammatory Diseases and Cancer Development.Frontiers in cell and developmental biology · 2019Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPlaque psoriasis is a non-contagious skin disease in which characteristic red and flaky lesions result from a dysregulation involving both innate and adaptive immune mechanisms. Several cytokines have been implicated in these processes and lately interleukin (IL)-36 family members have become more recognised among them. Thus far, genetic studies have only investigated IL36RN gene of this family in relation to pustular psoriasis. Since IL36G has previously demonstrated markedly increased levels in plaque psoriasis patients and is linked to IL-23/IL-17 axis critical in psoriasis pathology, it was chosen to be the focus of current report.
methodsEleven SNPs from IL36G region were genotyped in 728 plaque psoriasis patients and 320 healthy control individuals. Allele and haplotype frequencies between patients and controls were assessed by respective association tests. For more specific analyses, the patients were assigned into subgroups according to sex, age of disease onset, occurrence of psoriasis among relatives, seasonal aggravation, arthritis symptoms, body surface area (BSA) scores, and Psoriasis Area and Severity Index (PASI) scores.
resultsThe most significant results were obtained with SNPs rs28947206, rs28947207 and rs28947211 that were associated in entire plaque psoriasis analysis (multiple testing adjusted p value (p
conclusionsThe associated SNPs of this study or those in linkage disequilibrium with them could potentially affect the functionality of IL-36γ cytokine, which in turn may impact plaque psoriasis pathology. For instance, these variants could influence IL-36γ expression or 3D structure, thereby altering its ability to induce chemokine production in keratinocytes and various immune cells. The precise mechanisms of these actions are currently unknown and out of the scope of this study. To conclude, the present genetic association results confirm the proposed role of IL-36γ in plaque psoriasis development, with corresponding causal effects to be determined in forthcoming research.
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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.