Non-canonical signalling mediates changes in fungal cell wall PAMPs that drive immune evasion

Arnab Pradhan, Gabriela M. Avelar, Judith M. Bain, Delma Childers, Chloe Pelletier, Daniel E. Larcombe, Elena Shekhova, Mihai G. Netea, Gordon D. Brown, Lars Erwig, Neil A. R. Gow, Alistair J. P. Brown (Corresponding Author)

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To colonise their host, pathogens must counter local environmental and immunological challenges. We reveal that the fungal pathogen, Candida albicans, exploits diverse host signals to promote immune evasion via masking of the major pathogen associated molecular pattern (PAMP), β-glucan. Certain nutrients, stresses and antifungal drugs trigger β-glucan masking, whereas other inputs, such as nitrogen sources and quorum sensing molecules, exert limited effects on this PAMP. In particular, iron limitation triggers dramatic changes in the cell wall that reduce β-glucan exposure. This correlates with reduced phagocytosis by macrophages and attenuated cytokine responses by peripheral blood mononuclear cells. Iron limitation-induced β-glucan masking depends on parallel signalling via the iron transceptor Ftr1 and iron-responsive transcription factor Sef1, and the protein kinase A pathway. Our data reveal that C. albicans exploits a diverse range of specific host signals to trigger protective anticipatory responses against impending phagocytic attack and promote host colonisation.
Original languageEnglish
Article number5315
JournalNature Communications
Publication statusPublished - 22 Nov 2019



  • Candida albicans
  • immune evasion
  • cell wall
  • pathogen associated molecular patterns
  • β-glucan
  • iron responses
  • Ftr1
  • Sef1
  • cAMP-protein kinase A signalling

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