ArticleThe Journal of investigative dermatology2013
IL-1R1 signaling facilitates Munro's microabscess formation in psoriasiform imiquimod-induced skin inflammation.
Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 71 citations in OpenAlex.
- Calcium signaling in psoriasis: from pathogenesis to therapeutic opportunities.Frontiers in immunology · 2026Review
- Inflammaging and Senescence-Associated Secretory Phenotype (SASP) in Psoriasis - A Narrative Review of Potential Mechanisms and Anti-Inflammaging Strategies.Psoriasis (Auckland, N.Z.) · 2026Review
- Mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) as a novel topical immunomodulatory therapy for psoriasis: bridging the therapeutic gap in moderate disease.Extracellular vesicles and circulating nucleic acids · 2026Review
- Pathophysiology and Treatment of Psoriasis: From Clinical Practice to Basic Research.Pharmaceutics · 2025Review
- Human epidermis models demonstrate mediator role of TLR2 and TLR3 for psoriatic inflammation.Frontiers in medicine · 2025Article
- Article
- Adenosine and Its Receptors in the Pathogenesis and Treatment of Inflammatory Skin Diseases.International journal of molecular sciences · 2024Review
- Human neutrophils drive skin autoinflammation by releasing interleukin (IL)-26.The Journal of experimental medicine · 2024Article
- FloxedCells · 2024Article
- Crisaborole Inhibits Itch and Pain by Preventing Neutrophil Infiltration in a Mouse Model of Atopic Dermatitis.Acta dermato-venereologica · 2023Article
- FAM3C/ILEI protein is elevated in psoriatic lesions and triggers psoriasiform hyperproliferation in mice.EMBO molecular medicine · 2023Article
- IL-1Mediators of inflammation · 2023Review
- Calcium/calmodulin-dependent protein kinase IV promotes imiquimod-induced psoriatic inflammation via macrophages and keratinocytes in mice.Nature communications · 2022Article
- The Protective Role of pVHL in Imiquimod-Induced Psoriasis-like Skin Inflammation.International journal of molecular sciences · 2022Article
- Epidermis-Intrinsic Transcription Factor Ovol1 Coordinately Regulates Barrier Maintenance and Neutrophil Accumulation in Psoriasis-Like Inflammation.The Journal of investigative dermatology · 2022Article
- Transient Induction of Fever in the Imiquimod C57BL/6 Mouse Model of Psoriasis-Like Disease Involves IL-1 and IL-6 but Not IL-36.The Journal of investigative dermatology · 2022Article
- Genome-wide DNA methylation of Munro's microabscess reveals the epigenetic regulation in the pathogenesis of psoriasis.Frontiers in immunology · 2022Article
- The Extracellular Vesicles from the Commensal Staphylococcus Epidermidis ATCC12228 Strain Regulate Skin Inflammation in the Imiquimod-Induced Psoriasis Murine Model.International journal of molecular sciences · 2021Article
- Retinol and vitamin A metabolites accumulate through RBP4 and STRA6 changes in a psoriasis murine model.Nutrition & metabolism · 2020Article
- Metformin inhibits IL-1β secretion via impairment of NLRP3 inflammasome in keratinocytes: implications for preventing the development of psoriasis.Cell death discovery · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Munro's microabscesses contain polymorphonuclear leukocytes and form specifically in the epidermis of psoriasis patients. The mechanism whereby the neutrophils are recruited into the epidermis is poorly understood. Using a combination of human and mouse primary keratinocyte cell cultures and the imiquimod-induced psoriasis-like mouse model of skin inflammation, we explored the role of IL-1 signaling in microabscess formation. In vitro imiquimod stimulated production of IL-1α and neutrophil recruiting chemokines. Imiquimod-activated chemokine expression was dependent upon adenosine signaling and independent of IL-1α and IL-1 receptor type 1 (IL-1R1); nevertheless, IL-1α could enhance chemokine expression initiated by imiquimod. Topical application of imiquimod in vivo led to epidermal microabscess formation, acanthosis, and increased IL-1α and chemokine expression in the skin of wild-type mice. However, in IL-1R1-deficient mice these responses were either absent or dramatically reduced. These results demonstrate that IL-1α and IL-1R1 signaling is essential for microabscess formation, neutrophil recruiting chemokine expression, and acanthosis in psoriasis-like skin inflammation induced by imiquimod.
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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.