Psoriasis is a common chronic inflammatory skin disease mediated by innate and adaptive immune systems, characterized by abnormal proliferation and differentiation of epidermal keratinocytes and infiltration of inflammatory cells. Skin-specific keratinocytes are key participants in innate immunity, responding to immune cells and environmental stimulation, thereby serving an important role in the immunopathogenesis of psoriasis. Here, we present a method for inducing psoriasiform keratinocytes inflammation at transcription level with HaCaT cell line using five proinflammatory cytokines combination (M5 combination), including IL-17A, IL-22, IL-1α, TNF-α, and oncostatin M. Results demonstrate that M5 combination induced HaCaT cells showed increased levels of antimicrobial peptides (BD2, S100A7, S100A8, and S100A9), chemokines, and cytokines (CXCL1, CXCL2, CXCL8, CCL20, IL-1β, IL-6 and, IL-18). The mRNA levels of keratinocytes differentiation markers (Keratin1, Keratin10, Filaggrin, and Loricrin) were down regulated, which was consistent with the transcriptome data derived from psoriasis-like keratinocytes. The method described here, therefore, establishes an in vitro psoriasiform cutaneous inflammation at transcription level and contributes to the research for molecular pathogenesis of psoriasis.
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http://dx.doi.org/10.3791/61537 | DOI Listing |
Int J Mol Sci
December 2024
Research Laboratory of Surgery-Oncology, Department of Surgery, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Immunotherapy, particularly that based on blocking checkpoint proteins in many tumors, including melanoma, Merkel cell carcinoma, non-small cell lung cancer (NSCLC), triple-negative breast (TNB cancer), renal cancer, and gastrointestinal and endometrial neoplasms, is a therapeutic alternative to chemotherapy. Immune checkpoint inhibitor (ICI)-based therapies have the potential to target different pathways leading to the destruction of cancer cells. Although ICIs are an effective treatment strategy for patients with highly immune-infiltrated cancers, the development of different adverse effects including cutaneous adverse effects during and after the treatment with ICIs is common.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Dermatology, Duke University Medical Center, Durham, NC, USA.
Background: Psoriasiform dermatitis can be defined both clinically and histologically, but is not a traditionally recognized clinical or histologic diagnosis.
Objective: Analyze the final clinical diagnosis, demographics and clinical characteristics in patients with histologic psoriasiform dermatitis.
Methods: Retrospective cross-sectional analysis of patients with histologic psoriasiform dermatitis 2004-2017.
J Family Med Prim Care
November 2024
Department of Dermatology, Venereology and Leprosy, SRM Medical College and Research Centre, Chengalpattu, Tamil Nadu, India.
Systemic lupus erythematosus (SLE) is the prototype of an autoimmune disease with various manifestations in the skin and several other organs. Subacute cutaneous lupus erythematosus may present with annular and psoriasiform lesions. There have been case reports of pustular lesions in SLE.
View Article and Find Full Text PDFInt J Nanomedicine
December 2024
Laboratory of Chemical, Galenic and Pharmacological Development of Medicines (LR12ES09), Faculty of Pharmacy of Monastir, University of Monastir, Monastir, Tunisia.
Background: Phosphodiesterase-4 is an enzyme that regulates immune responses and contributes to the development of psoriasis. Dipyridamole and roflumilast function as phosphodiesterase-4 inhibitors, reducing pro-inflammatory cytokine expression. The aim was to evaluate the anti-psoriatic effect of the topical administration of dipyridamole and roflumilast nanoemulgel combination on imiquimod-induced psoriasiform skin inflammation in rats.
View Article and Find Full Text PDFJ Cutan Pathol
December 2024
Department of Dermatology and Pathology, University of California, California, USA.
Background: Erythroderma is a dermatologic condition characterized by widespread red and scaly skin. The causes include, but are not limited to, psoriasis, eczema, drug eruptions, pityriasis rubra pilaris (PRP), and cutaneous T-cell lymphoma. Most of these are typified by Type 2 (e.
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