ArticleJournal of immunology (Baltimore, Md. : 1950)2012
CIKS/Act1-mediated signaling by IL-17 cytokines in context: implications for how a CIKS gene variant may predispose to psoriasis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Enhanced meta-analysis and replication studies identify five new psoriasis susceptibility loci.Nature communications · 2015Pooled it
- Act1 drives chemoresistance via regulation of antioxidant RNA metabolism and redox homeostasis.The Journal of experimental medicine · 2024Article
- The star target in SLE: IL-17.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- TRAF3IP2-IL-17 Axis Strengthens the Gingival Defense against Pathogens.Journal of dental research · 2023Article
- Mechanisms of Corticosteroid Resistance in Type 17 Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The Role of Interleukin-17 in Juvenile Idiopathic Arthritis: From Pathogenesis to Treatment.Medicina (Kaunas, Lithuania) · 2022Review
- Shikonin inhibits CEBPD downregulation in IL‑17‑treated HaCaT cells and in an imiquimod‑induced psoriasis model.Molecular medicine reports · 2020Article
- IL-17 in inflammatory skin diseases psoriasis and hidradenitis suppurativa.Clinical and experimental immunology · 2020Review
- The IL-17 Family of Cytokines in Health and Disease.Immunity · 2019Review
- IL-17 integrates multiple self-reinforcing, feed-forward mechanisms through the RNA binding protein Arid5a.Science signaling · 2018Article
- Structure of a prokaryotic SEFIR domain reveals two novel SEFIR-SEFIR interaction modes.Journal of structural biology · 2018Article
- Interleukin 17 Family Cytokines: Signaling Mechanisms, Biological Activities, and Therapeutic Implications.Cold Spring Harbor perspectives in biology · 2018Review
- IL-17 Signaling: The Yin and the Yang.Trends in immunology · 2017Review
- MCPIP1/Regnase-1 Restricts IL-17A- and IL-17C-Dependent Skin Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Cardiac-restricted Overexpression of TRAF3 Interacting Protein 2 (TRAF3IP2) Results in Spontaneous Development of Myocardial Hypertrophy, Fibrosis, and Dysfunction.The Journal of biological chemistry · 2016Article
- IκBζ is a key driver in the development of psoriasis.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- CIKS/DDX3X interaction controls the stability of the Zc3h12a mRNA induced by IL-17.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Psoriasis drug development and GWAS interpretation through in silico analysis of transcription factor binding sites.Clinical and translational medicine · 2015Article
- IL-17 drives psoriatic inflammation via distinct, target cell-specific mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The differential regulation of human ACT1 isoforms by Hsp90 in IL-17 signaling.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Psoriasis is a relapsing skin disease characterized by abnormal keratinocyte proliferation and differentiation and by an influx of inflammatory immune cells. Recently, IL-17 cytokines have been strongly implicated as critical for the pathogenesis of this disease. IL-17A (also known as IL-17) and IL-17F are the signature cytokines of Th17 cells, but are also produced by innate cells, including γδ T cells present in skin, whereas epithelial cells, including keratinocytes, may produce IL-17C. IL-17 cytokines signal via the adaptor protein connection to IκB kinase and stress-activated protein kinases (CIKS)/Act1. Psoriasis is a disease with a strong genetic predisposition, and the gene encoding CIKS has recently been identified as a susceptibility locus. Unexpectedly, one predisposing gene variant features a mutation that impairs rather than enhances CIKS-mediated IL-17 cytokine signaling, counter to the predicted role for IL-17 cytokines in psoriatic inflammation. In this study, we demonstrate, however, that this mutant adaptor does not impair the IL-17-specific contributions to the genetic response when combined with TNF-α, a cytokine also prominent in psoriatic inflammation. Interestingly, TNF-α signals compensate IL-17 signaling defects imposed by this mutant adaptor even for genes that are not induced by TNF-α alone, including the transcription factors CCAAT/enhancer binding protein δ and IκBζ, which help regulate secondary gene expression in response to IL-17. Based on these findings we discuss a scenario in which the mutant adaptor may interfere with homeostatic maintenance of epithelial barriers, thereby potentially enabling the initiation of inflammatory responses to insults, whereas this same mutant adaptor would still be able to mediate IL-17-specific contributions to inflammation once TNF-α is present.
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Registered trials
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.