ArticleJournal of immunology (Baltimore, Md. : 1950)2009
IL-17 signaling for mRNA stabilization does not require TNF receptor-associated factor 6.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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.
The trial behind it
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
54 citing papers in PubMed, 86 citations in OpenAlex.
- Vunakizumab for IL-17A-Mediated Diseases: A Review in Psoriasis and Spondyloarthritis.Biologics : targets & therapy · 2026Review
- Review
- Review
- Dual interleukin-17A/F deficiency protects against acute and chronic response to cigarette smoke exposure in mice.Scientific reports · 2021Article
- From Bed to Bench and Back: TNF-α, IL-23/IL-17A, and JAK-Dependent Inflammation in the Pathogenesis of Psoriatic Synovitis.Frontiers in pharmacology · 2021Review
- 14-3-3ζ-TRAF5 axis governs interleukin-17A signaling.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- T Cell Cytokines Impact Epithelial Cell Responses duringJournal of immunology (Baltimore, Md. : 1950) · 2020Review
- TRAF1 suppresses antifungal immunity through CXCL1-mediated neutrophil recruitment during Candida albicans intradermal infection.Cell communication and signaling : CCS · 2020Article
- The Role of the Interleukin-17 Axis and Neutrophils in the Pathogenesis of Endemic and Systemic Mycoses.Frontiers in cellular and infection microbiology · 2020Review
- Interleukin-Mediated Pendrin Transcriptional Regulation in Airway and Esophageal Epithelia.International journal of molecular sciences · 2019Review
- IL-17R-EGFR axis links wound healing to tumorigenesis in Lrig1The Journal of experimental medicine · 2019Article
- TRAF Regulation of IL-17 Cytokine Signaling.Frontiers in immunology · 2019Review
- Immune Control by TRAF6-Mediated Pathways of Epithelial Cells in the EIME (Epithelial Immune Microenvironment).Frontiers in immunology · 2019Review
- Th17 response in patients with cervical cancer.Oncology letters · 2018Review
- IL-17 integrates multiple self-reinforcing, feed-forward mechanisms through the RNA binding protein Arid5a.Science signaling · 2018Article
- IL-17-receptor-associated adaptor Act1 directly stabilizes mRNAs to mediate IL-17 inflammatory signaling.Nature immunology · 2018Article
- IL-17 in Rheumatoid Arthritis and Precision Medicine: From Synovitis Expression to Circulating Bioactive Levels.Frontiers in medicine · 2018Review
- IL-17 in the lung: the good, the bad, and the ugly.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- IL-17 Signaling: The Yin and the Yang.Trends in immunology · 2017Review
- IL-17A enhances IL-13 activity by enhancing IL-13-induced signal transducer and activator of transcription 6 activation.The Journal of allergy and clinical immunology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
IL-17 alone is a relatively weak inducer of gene expression, but cooperates with other cytokines, including TNF-alpha, to generate a strong response in part via prolongation of mRNA t(1/2). Because TNFR-associated factor 6 (TRAF6) has been reported to be essential for signaling by IL-17, we examined its involvement in IL-17-mediated mRNA stabilization. Although overexpression of TRAF6 in HeLa cells activates NF-kappaB, it does not stabilize transfected KC mRNA. Furthermore, a dominant-negative TRAF6 abrogates NF-kappaB activation, but does not block IL-17-induced chemokine mRNA stabilization. IL-17 can stabilize KC and MIP-2 mRNAs comparably in TNF-alpha-treated mouse embryo fibroblasts from TRAF6(+/+) and TRAF6(-/-) mice. TRAF6 is known to couple upstream signals with activation of p38 MAPK and mitogen activated protein kinase activated protein kinase 2, both of which have been shown to be important for Toll/IL-1R-mediated mRNA stabilization in various cell types. Inhibition of p38 MAPK, however, does not block IL-17-induced KC mRNA stabilization, and IL-17 can stabilize KC mRNA equally in mouse embryo fibroblasts from both wild-type and mitogen activated protein kinase activated protein kinase 2/3 doubly-deficient mice. Finally, IL-17 can amplify the levels of multiple TNF-alpha-stimulated mRNAs in wild-type and TRAF6-deficient cells, but not in cells from Act1(-/-) mice. Collectively, these findings demonstrate the existence of a TRAF6/p38 MAPK-independent pathway that couples the IL-17R with enhanced mRNA stability. Because the most potent effects of IL-17 on gene expression are obtained in cooperation with other cytokines such as TNF-alpha, these findings suggest that this pathway is a major contributing mechanism for response to IL-17.
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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.