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DNAM-1 mediates NK-cell activation and host-pathogen interaction via direct binding to fungal cell wall proteases

Fariha Natasha1, Linda Heilig2, Dominic A Helmerich1

  • 1Department of Biotechnology & Biophysics (Biocenter), University of Wuerzburg, Wuerzburg, Germany.

Communications Biology
|April 13, 2026
PubMed

Insights

Natural killer (NK) cells use DNAX accessory molecule 1 (DNAM-1) to recognize fungal pathogens like Aspergillus and Candida. This interaction, mediated by fungal Sap10 protein, activates NK cells to combat invasive mycoses.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Natural killer (NK) cells are crucial for innate immunity against fungal infections.
  • Surface proteins on NK cells mediate interactions with microbial targets.
  • DNAX accessory molecule 1 (DNAM-1; CD226) is a key receptor on NK cells.

Purpose of the Study:

  • To investigate the role of DNAM-1 in NK cell recognition of Aspergillus fumigatus and Candida albicans hyphae.
  • To identify specific fungal ligands that bind to DNAM-1.
  • To elucidate the mechanism of NK cell activation by fungal pathogens via DNAM-1.

Main Methods:

  • Super-resolution microscopy to observe DNAM-1 distribution on NK cells.
  • Colony-forming assays to assess antifungal activity with and without DNAM-1 blocking.
  • In silico domain-domain interaction analysis to predict fungal DNAM-1 targets.
  • Co-immunoprecipitation and fluorescence correlation spectroscopy to confirm protein binding.
  • Flow cytometry to measure NK cell activation markers (CD69, perforin, CCL3).

Main Results:

  • DNAM-1 is uniformly distributed on NK cells and maintained upon fungal contact.
  • Blocking DNAM-1 reduced NK cell antifungal activity.
  • The fungal protein Sap10 (from C. albicans) was identified as a high-affinity DNAM-1 ligand.
  • Sap10 binding to NK cells induced their activation, characterized by increased CD69, perforin, and CCL3.

Conclusions:

  • DNAM-1 recognizes fungal pathogens, specifically binding to the Sap10 protein.
  • Sap10 acts as a fungal ligand for DNAM-1, mediating NK cell recognition and activation.
  • This study reveals a novel mechanism for NK cell-mediated immunity against invasive fungal infections.

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