ArticleCell death & disease2021
A novel function of NLRP3 independent of inflammasome as a key transcription factor of IL-33 in epithelial cells of atopic dermatitis.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- The parkin-γ-tubulin axis regulates epidermal homeostasis and is associated with the susceptibility to psoriasis.Cell death and differentiation · 2026Article
- Targeting ANGPTL3 and IL-33/ST2 Ameliorates Diabetic Kidney Disease by Reducing Lipotoxicity, Alleviating Inflammation and Inhibiting Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A combination therapy strategy: precision co-targeting of CCR7 and JAK1 with a smart hydrogel for inflammatory skin diseases.Journal of nanobiotechnology · 2026Article
- The Mechanism of NLRP3 Inflammasome Activation and Its Roles in Chronic Rhinosinusitis.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- Topical Trichosanthis Radix Water Extract Attenuates Atopic Dermatitis-Like Skin Inflammation: Marker Standardization, Network Pharmacology, and Preclinical Validation.Mediators of inflammation · 2026Article
- Interferon regulatory factor 4 as a context-dependent regulator of inflammation: transcriptional and epigenetic control, skin diseases, and translational challenges.Frontiers in immunology · 2026Review
- Extracellular vesicles in atopic dermatitis: unraveling pathogenic mediators and engineering therapeutic vectors.Frontiers in immunology · 2026Review
- Alleviation of Chitin- and Ovalbumin-Induced Steroid-Resistant Eosinophilic Airway Inflammation Associated with NLRP3 Axis Inhibition in a Mouse Model.Journal of inflammation research · 2026Article
- The expanding role of the NLRP3 inflammasome from periodic fevers to therapeutic targets.Nature immunology · 2025Review
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- SELEX (Systematic Evolution of Ligands by Exponential Enrichment) to Identify DNA Motifs Mirroring Chromosome Targets of the Hypothetical Transcription Factor NLRP3.Methods in molecular biology (Clifton, N.J.) · 2025Article
- NLRP3 regulates epithelial barrier integrity and protects from airway hyperresponsiveness in experimental allergic asthma.Frontiers in immunology · 2025Article
- The regulatory effects of luteolin, calycosin, and formononetin on the NLRP3/IL-33/ILC2s axis in the treatment of allergic rhinitis: mechanistic analysis and therapeutic potential.Frontiers in pharmacology · 2025Review
- Cannabichromene as a Novel Inhibitor of Th2 Cytokine and JAK/STAT Pathway Activation in Atopic Dermatitis Models.International journal of molecular sciences · 2024Article
- The NLRP3 inflammasome in allergic diseases: mechanisms and therapeutic implications.Clinical and experimental medicine · 2024Review
- Mitochondrial GRIM19 Loss Induces Liver Fibrosis through NLRP3/IL33 Activation via Reactive Oxygen Species/NF-кB Signaling.Journal of clinical and translational hepatology · 2024Article
- Cutaneous inflammasome driving ASC / gasdermin-D activation and IL-1β-secreting macrophages in severe atopic dermatitis.Archives of dermatological research · 2024Article
- Associations ofHeliyon · 2024Article
- Multi-Omics Approach to Improved Diagnosis and Treatment of Atopic Dermatitis and Psoriasis.International journal of molecular sciences · 2024Review
- Effect of Chloroquine on Type 2 Inflammatory Response in MC903-Induced Atopic Dermatitis Mice.Clinical, cosmetic and investigational dermatology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Atopic dermatitis (AD) is a common chronic pruritic inflammatory skin disorder characterized by recurrent eczematous lesions. Interleukin (IL)-33, a cytokine of the IL-1 family, was found to play an important role in the pathogenesis of AD. As a key component of the inflammasome, NLRP3 has been mostly described in myeloid cells that to mediate inflammasome activation conducted proinflammatory cytokine production of the IL-1 family. However, the role of NLRP3 inflammasome in the pathogenesis of AD, as well as IL-33 processing are highly controversial. Whether NLRP3 can mediate IL-33 expression and secretion independently of the inflammasome in the epithelium of AD has remained unclear. In this article, we found the mRNA expression of Il33 and Nlrp3 were notably increased in the lesional skin of AD patients compared to healthy controls. We then found a significant positive correlation between the expression of Nlrp3 and Il33 in the epithelium of MC903-mediated AD mice model, but no changes were observed for Il36α, Il36γ, Il1β, or Il18 mRNA expression, as well as IL-1β or IL-18 production. Overexpression of NLRP3 in human immortalized epithelial cells increased IL-33 expression, whereas siRNA targeting NLRP3 abolished IL-33 expression. In addition, inhibition of NLRP3 inflammasome activation or caspase-1 activity with MCC950 or VX-765 showed no effect on the expression and secretion of IL-33 in AD mice. Unlike myeloid cells, NLRP3 predominantly located in the nucleus of epithelial cells, which could directly bind to Il33 specific-promoters and transactivate it through an interaction with transcription factor IRF4. Furthermore, NLRP3 deficient mice exhibited a significant alleviated epidermis inflammation and decreased mRNA expression and secretion of IL-33 in MC903-mediated AD mice without interfering with TSLP and IL-1β production. Our results demonstrate a novel ability of NLRP3 to function as a crucial transcription factor of IL-33 in epithelium independently of inflammasome that to mediate the pathological process of AD.
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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.