ArticleThe Journal of investigative dermatology2015
Unprocessed Interleukin-36α Regulates Psoriasis-Like Skin Inflammation in Cooperation With Interleukin-1.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
The trial behind it
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Differential Expression of IL-36 Family Members and IL-38 by Immune and Nonimmune Cells in Patients with Active Inflammatory Bowel Disease.BioMed research international · 2018Trial
- FloxedCells · 2024Article
- Serum Interleukin-36 α as a Candidate Biomarker to Distinguish Behçet's Syndrome and Psoriatic Arthritis.International journal of molecular sciences · 2023Article
- The role of the interleukin-36 axis in generalized pustular psoriasis: a review of the mechanism of action of spesolimab.Frontiers in immunology · 2023Review
- Epidermis-Intrinsic Transcription Factor Ovol1 Coordinately Regulates Barrier Maintenance and Neutrophil Accumulation in Psoriasis-Like Inflammation.The Journal of investigative dermatology · 2022Article
- Advances in the pathogenesis of psoriasis: from keratinocyte perspective.Cell death & disease · 2022Review
- IL-36 is Closely Related to Neutrophilic Inflammation in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2022Article
- Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model.Cell and tissue research · 2021Article
- Epidermal PPARγ Is a Key Homeostatic Regulator of Cutaneous Inflammation and Barrier Function in Mouse Skin.International journal of molecular sciences · 2021Article
- Immune responses and therapeutic options in psoriasis.Cellular and molecular life sciences : CMLS · 2021Review
- IL-36 in chronic inflammation and fibrosis - bridging the gap?The Journal of clinical investigation · 2021Review
- IL-1 Family Antagonists in Mouse and Human Skin Inflammation.Frontiers in immunology · 2021Review
- IL-36 signaling in keratinocytes controls early IL-23 production in psoriasis-like dermatitis.Life science alliance · 2020Article
- Keratinocyte interleukin-36 receptor expression orchestrates psoriasiform inflammation in mice.Life science alliance · 2020Article
- Interleukin-36 family dysregulation drives joint inflammation and therapy response in psoriatic arthritis.Rheumatology (Oxford, England) · 2020Article
- IL-36 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- IL-36α Promoted Wound Induced Hair Follicle Neogenesis via Hair Follicle Stem/Progenitor Cell Proliferation.Frontiers in cell and developmental biology · 2020Article
- Evidence for a role of autoinflammation in early-phase psoriasis.Clinical and experimental immunology · 2019Article
- IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners.Nature communications · 2019Article
- The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Generalized pustular psoriasis is a severe skin disease characterized by epidermal hyperplasia, neutrophil-rich abscesses within the epidermis, and a mixed inflammatory infiltrate in the dermis. The disease may be caused by missense mutations in the IL-36 receptor antagonist, IL-36Ra. Curiously, the related IL-1Ra has therapeutic effects in some of these latter patients. Here, using an experimental mouse model of psoriasiform skin inflammation, we demonstrate in vivo connections between IL-36 and IL-1 expression. After disease initiation, IL-36α-deficient mice exhibited dramatically diminished skin pathology, including absence of epidermal neutrophils, reduced keratinocyte acanthosis, and less dermal edema. In contrast, IL-36β and IL-36γ knockout mice developed disease indistinguishable from that of wild-type mice. The endogenous IL-36α was not processed through proteolysis. Although IL-36α expression was strongly induced in an IL-1 signaling-dependent manner during disease, expression of IL-1α was also dependent upon IL-36α. Hence, after being upregulated by IL-1α, IL-36α acts through a feedback mechanism to boost IL-1α levels. Analyses of double knockout mice further revealed that IL-36α and IL-1α cooperate to promote psoriasis-like disease. In conclusion, IL-1α and IL-36α form a self-amplifying inflammatory loop in vivo that in patients with insufficient counter regulatory mechanisms may become hyper-engaged and/or chronic.
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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.