ArticleJournal of immunology (Baltimore, Md. : 1950)2010
IL-17RC is required for immune signaling via an extended SEF/IL-17R signaling domain in the cytoplasmic tail.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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.
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Who cites it
75 citing papers in PubMed, 122 citations in OpenAlex.
- Candidalysin promotes fungal-specific Th17 CD4 T cell differentiation and protective systemic immunogenicity.Mucosal immunology · 2026Article
- Combinatorial actions of IL-22 and IL-17 drive optimal immunity to oral candidiasis through SPRRs.PLoS pathogens · 2024Article
- Isolated Chronic Mucocutaneous Candidiasis due to a Novel Duplication Variant of IL17RC.Journal of clinical immunology · 2023Article
- IκBζ is an essential mediator of immunity to oropharyngeal candidiasis.Cell host & microbe · 2023Article
- SARS-CoV-2 ORF8 Mediates Signals in Macrophages and Monocytes through MyD88 Independently of the IL-17 Receptor.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Immune-Epithelial Cross Talk in Regeneration and Repair.Annual review of immunology · 2023Review
- Pathogenesis and virulence ofVirulence · 2022Review
- Radiation Exposure Perturbs IL-17RA-Mediated Immunity Leading to Changes in Neutrophil Responses That Increase Susceptibility to Oropharyngeal Candidiasis.Journal of fungi (Basel, Switzerland) · 2022Article
- Infections in the monogenic autoimmune syndrome APECED.Current opinion in immunology · 2021Review
- Tissue-resident memory Th17 cells maintain stable fungal commensalism in the oral mucosa.Mucosal immunology · 2021Article
- An IL-17F.S65L Knock-In Mouse Reveals Similarities and Differences in IL-17F Function in Oral Candidiasis: A New Tool to Understand IL-17F.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Oral epithelial IL-22/STAT3 signaling licenses IL-17-mediated immunity to oral mucosal candidiasis.Science immunology · 2020Article
- Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity.Science immunology · 2020Review
- The IL-23/IL-17 Pathway in Inflammatory Skin Diseases: From Bench to Bedside.Frontiers in immunology · 2020Review
- New Insights inFrontiers in cellular and infection microbiology · 2020Review
- Article
- Immune Cell Production of Interleukin 17 Induces Stem Cell Features of Pancreatic Intraepithelial Neoplasia Cells.Gastroenterology · 2018Article
- Mucocutaneous IL-17 immunity in mice and humans: host defense vs. excessive inflammation.Mucosal immunology · 2018Review
- Candida albicans-epithelial interactions and induction of mucosal innate immunity.Current opinion in microbiology · 2017Review
- Oral epithelial cells orchestrate innate type 17 responses toScience immunology · 2017Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
IL-17 mediates essential inflammatory responses in host defense and autoimmunity. The IL-17A-IL-17F signaling complex is composed of IL-17RA and IL-17RC, both of which are necessary for signal transduction. To date, the specific contribution of IL-17RC to downstream signaling remains poorly understood. To define the regions within the IL-17RC cytoplasmic tail required for signal transduction, we assayed signaling by a panel of IL-17RC deletion mutants. These findings reveal that IL-17RC inducibly associates with a specific glycosylated IL-17RA isoform, in a manner independent of the IL-17RC cytoplasmic tail. Using expression of the IL-17 target genes IL-6 and 24p3/lipocalin-2 as a readout, functional reconstitution of signaling in IL-17RC(-/-) fibroblasts required the SEF/IL-17R signaling domain (SEFIR), a conserved motif common to IL-17R family members. Unexpectedly, the IL-17RC SEFIR alone was not sufficient to reconstitute IL-17-dependent signaling. Rather, an additional sequence downstream of the SEFIR was also necessary. We further found that IL-17RC interacts directly with the adaptor/E3 ubiquitin ligase Act1, and that the functional IL-17RC isoforms containing the extended SEFIR region interact specifically with a phosphorylated isoform of Act1. Finally, we show that IL-17RC is required for in vivo IL-17-dependent responses during oral mucosal infections caused by the human commensal fungus Candida albicans. These results indicate that IL-17RC is vital for IL-17-dependent signaling both in vitro and in vivo. Insight into the mechanisms by which IL-17RC signals helps shed light on IL-17-dependent inflammatory responses and may ultimately provide an avenue for therapeutic intervention in IL-17-mediated diseases.
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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.