ArticleEMBO molecular medicine2021
Psoriatic skin inflammation is promoted by c-Jun/AP-1-dependent CCL2 and IL-23 expression in dendritic cells.
Article in EMBO molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Histone and Histone Acetylation-Related Alterations of Gene Expression in Uninvolved Psoriatic Skin and Their Effects on Cell Proliferation, Differentiation, and Immune Responses.International journal of molecular sciences · 2023Pooled it
- The genesis of cutaneous neurogenic inflammation is a multi-step process requiring dendritic cell aggregation.Immunity · 2026Article
- Single-Cell Transcriptomics Reveals the Immune Pathogenesis of Isolated Coronary Arteritis Presenting as Refractory In-Stent Restenosis.JACC. Basic to translational science · 2026Article
- Article
- Wogonin as a potential therapeutic agent for psoriasis: Core target identification and validation.Experimental and therapeutic medicine · 2026Article
- Cutaneous Dendritic Cells: Structure, Function and Immune Role.Biomedicines · 2026Review
- Targeting KAT8 alleviates self-RNA-driven skin inflammation by modulating histone H4 lysine 16 acetylation in psoriasis.Cell death and differentiation · 2026Article
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Comprehensive profiling of immune cell infiltration and biomarker identification in intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2025Article
- JNK/c-Jun cascade activation enhances malignant proliferation of psoriatic keratinocytes by regulating ROS levels and mitochondrial membrane potential.European journal of medical research · 2025Article
- Lobetyolin alleviates IMQ‑induced psoriasis‑like skin inflammation by maintaining the homeostasis of the skin and inhibiting the inflammatory cytokines in dendritic cells.International journal of molecular medicine · 2025Article
- Biochanin A Ameliorates Imiquimod-Induced Psoriasis-Like Skin Inflammation in Mice by Modulating the NF-κB and MAPK Signaling Pathways.Inflammation · 2025Article
- A drug delivery perspective on nanotechnology-based topical therapeutics for inflammatory skin diseases.Nanomedicine (London, England) · 2025Review
- MAPK15 PreventsInternational journal of molecular sciences · 2025Article
- B cell-derived acetylcholine mitigates skin inflammation in mice through α9 nicotinic acetylcholine receptor-mediated signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Topical TYK2 inhibitor ameliorates psoriasis-like dermatitis via the AKT-SP1-NGFR-AP1 pathway in keratinocytes.Clinical and translational medicine · 2025Article
- Celastrol directly targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression.Acta pharmaceutica Sinica. B · 2025Article
- Systemic IFN-I combined with topical TLR7/8 agonists promotes distant tumor suppression by c-Jun-dependent IL-12 expression in dendritic cells.Nature cancer · 2025Article
- Identification and Validation of Hub Genes in Hidradenitis Suppurativa.Clinical, cosmetic and investigational dermatology · 2025Article
- Chaperone-mediated autophagy dysfunction in imiquimod-induced psoriasiform dermatitis.Autophagy reports · 2025Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Toll-like receptor (TLR) stimulation induces innate immune responses involved in many inflammatory disorders including psoriasis. Although activation of the AP-1 transcription factor complex is common in TLR signaling, the specific involvement and induced targets remain poorly understood. Here, we investigated the role of c-Jun/AP-1 protein in skin inflammation following TLR7 activation using human psoriatic skin, dendritic cells (DC), and genetically engineered mouse models. We show that c-Jun regulates CCL2 production in DCs leading to impaired recruitment of plasmacytoid DCs to inflamed skin after treatment with the TLR7/8 agonist Imiquimod. Furthermore, deletion of c-Jun in DCs or chemical blockade of JNK/c-Jun signaling ameliorates psoriasis-like skin inflammation by reducing IL-23 production in DCs. Importantly, the control of IL-23 and CCL2 by c-Jun is most pronounced in murine type-2 DCs. CCL2 and IL-23 expression co-localize with c-Jun in type-2/inflammatory DCs in human psoriatic skin and JNK-AP-1 inhibition reduces the expression of these targets in TLR7/8-stimulated human DCs. Therefore, c-Jun/AP-1 is a central driver of TLR7-induced immune responses by DCs and JNK/c-Jun a potential therapeutic target in psoriasis.
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