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Updated: Jul 16, 2025

Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
08:02

Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice

Published on: February 18, 2015

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IκBζ is an essential mediator of immunity to oropharyngeal candidiasis

Tiffany C Taylor1, Bianca M Coleman1, Samyuktha P Arunkumar1

  • 1Division of Rheumatology & Clinical Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA.

Cell Host & Microbe
|September 19, 2023
PubMed

Insights

A key transcription factor, IκBζ, is crucial for mucosal immunity against fungal Candida albicans infections. It works with Egr3 to activate antimicrobial peptides, offering a new target for antifungal therapies.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Fungal infections pose a global health challenge with no existing vaccines.
  • T-helper 17 (Th17) cells are vital for immunity against Candida albicans, but downstream pathways are not fully understood.

Purpose of the Study:

  • To elucidate the downstream mechanisms of Th17-mediated immunity against oropharyngeal candidiasis (OPC).
  • To investigate the role of IκBζ (Nfkbiz) in mucosal defense against fungal pathogens.

Main Methods:

  • Murine model of oropharyngeal candidiasis.
  • Gene deletion studies targeting Nfkbiz.
  • Analysis of gene expression, including beta-defensins (BD3/DEFB4A).
  • Investigation of transcription factor interactions (IκBζ and Egr3).

Main Results:

  • IκBζ was upregulated in an IL-17-dependent manner and essential for preventing candidiasis in mice.
  • Deletion of Nfkbiz led to increased susceptibility to OPC.
  • IκBζ regulated the antimicrobial peptide beta-defensin 3 (BD3) and its human ortholog DEFB4A.
  • IκBζ controlled Egr3, which was critical for inducing DEFB4A in response to Candida albicans.

Conclusions:

  • IκBζ acts in oral epithelial cells, not hematopoietic cells, to control OPC.
  • IκBζ and Egr3 form a critical antifungal signaling hub for mucosal defense.
  • This pathway represents a potential target for developing new antifungal strategies.
Keywords:
Candida albicansIL-17 signalingcytokinesdefensinsoral epitheliumsignal transduction

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