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<p>Oropharyngeal candidiasis (OPC) poses a significant health threat, yet the single-cell transcriptomic landscape of immune factors involved in its pathogenesis remains unexplored. By employing single-cell RNA sequencing in murine models of OPC, we illuminated the immune dynamics and heterogeneity within this niche. We observed an accumulation of monocyte-derived TREM2<sup>+</sup> (triggering receptor expressed on myeloid cells-2) macrophages following <i>Candida albicans</i> infection. These macrophages exhibit pro-inflammatory properties and help regulate protective antifungal immunity. Mechanistically, TREM2 recognizes candidalysin at G65, N73, and N91-K92, triggering DAP12 signaling and resulting in the production of TNF-α. This contributes to the early activation of neutrophil and macrophage antifungal functions. Importantly, these processes are driven by TREM2-mediated TNF-α signaling, which specifically depends on the recognition of candidalysin. Collectively, our findings reveal that TREM2 acts as a potential receptor for candidalysin, mediating the intricate host–pathogen interaction that drives antifungal immunity in the oral mucosa.</p>

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TREM2-mediated recognition of candidalysin by macrophages confers early protective innate immunity in oropharyngeal candidiasis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月18日

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  • Weiwei Deng,
  • Yishan Chen,
  • Kai Zhang,
  • Siqi Liu,
  • Kefan Lin,
  • Jun Zhang,
  • Yi Zhang,
  • Di Wang,
  • Ruoyu Li,
  • Xiaowen Wang,
  • Yingping Xu,
  • Yunsheng Liang

摘要

Oropharyngeal candidiasis (OPC) poses a significant health threat, yet the single-cell transcriptomic landscape of immune factors involved in its pathogenesis remains unexplored. By employing single-cell RNA sequencing in murine models of OPC, we illuminated the immune dynamics and heterogeneity within this niche. We observed an accumulation of monocyte-derived TREM2+ (triggering receptor expressed on myeloid cells-2) macrophages following Candida albicans infection. These macrophages exhibit pro-inflammatory properties and help regulate protective antifungal immunity. Mechanistically, TREM2 recognizes candidalysin at G65, N73, and N91-K92, triggering DAP12 signaling and resulting in the production of TNF-α. This contributes to the early activation of neutrophil and macrophage antifungal functions. Importantly, these processes are driven by TREM2-mediated TNF-α signaling, which specifically depends on the recognition of candidalysin. Collectively, our findings reveal that TREM2 acts as a potential receptor for candidalysin, mediating the intricate host–pathogen interaction that drives antifungal immunity in the oral mucosa.