ArticleCell host & microbe2023
IκBζ is an essential mediator of immunity to oropharyngeal candidiasis.
Article in Cell host & microbe, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- IL-1 family signalling drives mucosal defence against systemic Candida albicans infection.Nature microbiology · 2026Article
- IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Non-canonical IL‑22 receptor signaling remodels the oral mucosal barrier during Candida albicans immunosurveillance.Nature communications · 2026Article
- Streptococcus salivarius CCFM1416 Modulates Oral Immunity via IL-17/IKBζ and Combats Candida albicans Infection.Probiotics and antimicrobial proteins · 2026Article
- Transcriptomic characterization of key psoriasis-associated genes based on single-cell RNA-seq and machine learning.PloS one · 2026Article
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- Fungal pathogen-responsive Th17 cells in gut-mouth axis enhance protection against oropharyngeal candidiasis.iScience · 2025Article
- GM-CSF-mediated epithelial-immune cell cross-talk orchestrates pulmonary immunity toScience immunology · 2025Article
- Neutrophils in nasal polyps exhibit transcriptional adaptation and proinflammatory roles that depend on local polyp milieu.JCI insight · 2024Article
- 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
- Epithelial responses to fungal pathogens.Current opinion in microbiology · 2024Review
- Combinatorial actions of IL-22 and IL-17 drive optimal immunity to oral candidiasis through SPRRs.PLoS pathogens · 2024Article
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11 authors at 2 institutions in 1 country.
Funding
Abstract
Fungal infections are a global threat; yet, there are no licensed vaccines to any fungal pathogens. Th17 cells mediate immunity to Candida albicans, particularly oropharyngeal candidiasis (OPC), but essential downstream mechanisms remain unclear. In the murine model of OPC, IκBζ (Nfkbiz, a non-canonical NF-κB transcription factor) was upregulated in an interleukin (IL)-17-dependent manner and was essential to prevent candidiasis. Deletion of Nfkbiz rendered mice highly susceptible to OPC. IκBζ was dispensable in hematopoietic cells and acted partially in the suprabasal oral epithelium to control OPC. One prominent IκBζ-dependent gene target was β-defensin 3 (BD3) (Defb3), an essential antimicrobial peptide. Human oral epithelial cells required IκBζ for IL-17-mediated induction of BD2 (DEFB4A, human ortholog of mouse Defb3) through binding to the DEFB4A promoter. Unexpectedly, IκBζ regulated the transcription factor Egr3, which was essential for C. albicans induction of BD2/DEFB4A. Accordingly, IκBζ and Egr3 comprise an antifungal signaling hub mediating mucosal defense against oral candidiasis.
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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.