ArticleJournal of translational medicine2022
IL-32 promotes the occurrence of atopic dermatitis by activating the JAK1/microRNA-155 axis.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- The Emerging Role of Interleukin-32 in HIV-Associated Cardiovascular Comorbidities: A Mini Review.International journal of general medicine · 2026Review
- Expression of MicroRNA-155 and its associations with EBV serological markers and inflammatory cytokines in young lymphoma patients with evidence of active EBV infection.Experimental biology and medicine (Maywood, N.J.) · 2026Observational
- Elevated Serum Levels of miRNA-155 in Children with Atopic Dermatitis: A Potential Biomarker of Disease.International journal of molecular sciences · 2025Article
- Mini review: Interleukin-32 as a key mediator of type 1 diabetes pathogenesis.Frontiers in immunology · 2025Review
- Identification of potential miR‑155 target genes in epidermal immune microenvironment of atopic dermatitis patients and their inflammatory effects on HaCaT cells.Experimental and therapeutic medicine · 2024Article
- Intrinsic Effects of Exposome in Atopic Dermatitis: Genomics, Epigenomics and Regulatory Layers.Journal of clinical medicine · 2023Review
- IL-32 as a potential biomarker and therapeutic target in skin inflammation.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aims to explore the mechanism of interleukin-32 (IL-32) affecting atopic dermatitis (AD) through the Janus-activated kinase-1 (JAK1)/microRNA-155 (miR-155) axis.
methodsIn this study, skin tissue samples and blood samples from normal subjects and patients with AD, human immortalized keratinocytes (HaCaT), and PA-induced mouse models of AD were selected for expression determination of IL-32, JAK1 and miR-155. The interaction among IL-32, JAK1 and miR-155 was identified with their roles in AD analyzed through loss- and gain-of-function assays.
resultsElevated IL-32 was detected in AD tissues and blood samples and promoted the occurrence of AD. IL-32 upregulated JAK1 expression and phosphorylation of its downstream genes, thus activating the JAK signaling pathway. JAK1 promoted the expression of miR-155. IL-32/JAK1/miR-155 axis promoted inflammation in the AD skin reconstruction model. In vivo experiments further confirmed that IL-32 promoted AD development by activating the JAK1/miR-155 axis.
conclusionThe present study underlined that IL-32 promoted the occurrence of AD by promoting JAK1 expression to upregulate miR-155 expression.
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