ArticleProceedings of the National Academy of Sciences of the United States of America2015
IκBζ is a key driver in the development of psoriasis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed.
- Elevated serum cardiotrophin-1 and interleukin-17 levels in psoriasis.Irish journal of medical science · 2026Article
- Olive (Olea europaea) phenolics for the control of psoriasis via targeting SMYD2 and IL-17A protein-protein interaction networks.Journal of natural medicines · 2026Article
- Plant extract mixture shows anti-inflammatory and barrier-strengthening effects and activates aryl hydrocarbon receptor in a 2D psoriasis model.Scientific reports · 2026Article
- Functional segregation of HIF-1α and AhR controls NK cell responsiveness under hypoxia.iScience · 2026Article
- IL-17 Cytokines Induce IκBζ in Dermal Fibroblasts to Promote Pro-Inflammatory Gene Expression in Psoriasis.International journal of molecular sciences · 2026Article
- The IL-1R and NFKBIZ pathway mediates immunoregulatory responses and immunotherapy efficacy in anaplastic large cell lymphoma.Leukemia · 2026Article
- Epithelial Regnase-1 inhibits colorectal tumor growth by regulating IL-17 signaling via degradation ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Determination of IL-17, BCL-3 and IκBζ expression levels in the gingival crevicular fluid of psoriasis patients.Archives of dermatological research · 2025Observational
- Interventions in cytokine signaling: novel horizons for psoriasis treatment.Frontiers in immunology · 2025Review
- The RNA binding protein Arid5a drives IL-17-dependent autoantibody-induced glomerulonephritis.The Journal of experimental medicine · 2024Article
- The Nuclear NF-κB Regulator IκBζ: Updates on Its Molecular Functions and Pathophysiological Roles.Cells · 2024Review
- IκBζ is a dual-use coactivator of NF-κB and POU transcription factors.Molecular cell · 2024Article
- Suppression of TCF4 promotes a ZC3H12A-mediated self-sustaining inflammatory feedback cycle involving IL-17RA/IL-17RE epidermal signaling.JCI insight · 2024Article
- Targeted siRNA Therapy for Psoriasis: Translating Preclinical Potential into Clinical Treatments.ImmunoTargets and therapy · 2024Review
- IκBζ is an essential mediator of immunity to oropharyngeal candidiasis.Cell host & microbe · 2023Article
- Cross-talk of inflammation and chondrocyte intracellular metabolism in osteoarthritis.Osteoarthritis and cartilage · 2023Review
- Pharmacogenomics on the Treatment Response in Patients with Psoriasis: An Updated Review.International journal of molecular sciences · 2023Review
- IL-17A and TNF synergistically drive expression of proinflammatory mediators in synovial fibroblasts via IκBζ-dependent induction of ELF3.Rheumatology (Oxford, England) · 2023Article
- The central inflammatory regulator IκBζ: induction, regulation and physiological functions.Frontiers in immunology · 2023Review
- Cytokine Modulators in Plaque Psoriasis - A Review of Current and Prospective Biologic Therapeutic Approaches.JAAD international · 2022Review
7 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a common immune-mediated, chronic, inflammatory skin disease characterized by hyperproliferation and abnormal differentiation of keratinocytes and infiltration of inflammatory cells. Although TNFα- and IL-17A-targeting drugs have recently proven to be highly effective, the molecular mechanism underlying the pathogenesis of psoriasis remains poorly understood. We found that expression of the atypical IκB member IκB (inhibitor of NF-κB) ζ, a selective coactivator of particular NF-κB target genes, was strongly increased in skin of patients with psoriasis. Moreover, in human keratinocytes IκBζ was identified as a direct transcriptional activator of TNFα/IL-17A-inducible psoriasis-associated proteins. Using genetically modified mice, we found that imiquimod-induced psoriasis-like skin inflammation was completely absent in IκBζ-deficient mice, whereas skin inflammation was still inducible in IL-17A- and TNFα-deficient mice. IκBζ deficiency also conferred resistance against IL-23-induced psoriasis. In addition, local abrogation of IκBζ function by intradermal injection of IκBζ siRNA abolished psoriasis-like skin inflammation. Taken together, we identify IκBζ as a hitherto unknown key regulator of IL-17A-driven effects in psoriasis. Thus, targeting IκBζ could be a future strategy for treatment of psoriasis, and other inflammatory diseases for which IL-17 antagonists are currently tested in clinical trials.
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