ArticleThe Journal of biological chemistry2011
Tumor necrosis factor α-mediated induction of interleukin 17C in human keratinocytes is controlled by nuclear factor κB.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 63 citations in OpenAlex.
- Therapeutic targeting of interleukin-17C signaling in carcinogenesis of endometriosis.Cell reports. Medicine · 2025Article
- Role of IL-17 cytokines in tubal fibrosis and infertility due to salpingitis.Molecular biology reports · 2025Review
- Human bladder organoids model urinary tract infection and bacteriophage therapy.bioRxiv : the preprint server for biology · 2025Article
- Mechanisms and safety evaluation of stir-fried atractylodis macrocephalae rhizoma with aurantii fructus in the treatment of inflammatory bowel disease: a study based on organ-on-a-chip model.Frontiers in pharmacology · 2025Article
- Suppression of TCF4 promotes a ZC3H12A-mediated self-sustaining inflammatory feedback cycle involving IL-17RA/IL-17RE epidermal signaling.JCI insight · 2024Article
- IL-17 Inhibition: A Valid Therapeutic Strategy in the Management of Hidradenitis Suppurativa.Pharmaceutics · 2023Review
- IL-17C neutralization protects the kidney against acute injury and chronic injury.EBioMedicine · 2023Article
- Phase 1 and 2 Randomized Clinical Studies Determine Lack of Efficacy for Anti-IL-17C Antibody MOR106 in Moderate-Severe Atopic Dermatitis.Journal of clinical medicine · 2022Article
- Th17-Derived Cytokines Synergistically Enhance IL-17C Production by the Colonic Epithelium.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Review
- Review
- IL-17C and IL-17RE Promote Wound Closure in aMicroorganisms · 2021Article
- LncRNA UCA1 negatively regulates NF-kB activity in psoriatic keratinocytes through the miR125a-A20 axis.The Kaohsiung journal of medical sciences · 2021Article
- A Novel Sample Selection Approach to Aid the Identification of Factors That Correlate With the Control of HIV-1 Infection.Frontiers in immunology · 2021Article
- IL-17 in inflammatory skin diseases psoriasis and hidradenitis suppurativa.Clinical and experimental immunology · 2020Review
- IL-17C/IL-17RE: Emergence of a Unique Axis in TFrontiers in immunology · 2020Review
- NFKBIZ and CW6 in Adalimumab Response Among Psoriasis Patients: Genetic Association and Alternative Transcript Analysis.Molecular diagnosis & therapy · 2019Article
- Gene Variant in the NF-BioMed research international · 2019Article
- The roles of IL-17C in T cell-dependent and -independent inflammatory diseases.Scientific reports · 2018Article
- The IL-17 Family of Cytokines in Psoriasis: IL-17A and Beyond.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-17C is a member of the IL-17 family of cytokines. The expression of IL-17C has been demonstrated to be strongly induced by TNFα in human keratinocytes, and recently the level of IL-17C was found to be increased in the inflammatory skin disease psoriasis. However, little is known about the molecular mechanisms involved in the regulation of IL-17C. Here, we show that pretreatment of cultured human keratinocytes with the inhibitor of κB kinase 2 inhibitor, SC-514, resulted in a significant reduction in both IL-17C mRNA and protein expression, indicating the significance of this pathway in the regulation of IL-17C. NF-κB binding sites were identified upstream from the IL-17C gene, and by electrophoretic mobility shift assay NF-κB was shown to bind to all three identified binding sites. Moreover, NF-κB binding to these sites was inducible by TNFα. Supershift analysis revealed binding of the NF-κB subunits p65 and p50 to all three NF-κB binding sites. To determine the contribution of NF-κB in IL-17C expression, we conducted luciferase gene reporter experiments and demonstrated that a 3204-bp promoter fragment of IL-17C containing three putative NF-κB binding sites was strongly activated by TNFα. Interestingly, mutations of the three NF-κB binding sites revealed that one specific NF-κB binding site was crucial for the TNFα-mediated IL-17C induction because mutation of this specific site completely abolished TNFα-induced IL-17C promoter activation. We conclude that the activation of NF-κB (p65/p50) is crucial for the TNFα-induced stimulation of IL-17C expression in human keratinocytes.
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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.