ArticleCommunications biology2026
DNAM-1 mediates NK-cell activation and host-pathogen interaction via direct binding to fungal cell wall proteases.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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15 authors.
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Abstract
Natural killer (NK) cells play a key role in combating invasive mycoses, with surface proteins crucial for immune cell-target interactions. Here, we investigate the role of DNAX accessory molecule 1 (DNAM-1; CD226) in the recognition of Aspergillus fumigatus and Candida albicans hyphae. Super-resolution microscopy reveals a uniform distribution of DNAM-1 on naïve NK cells that is maintained upon contact with fungal hyphae. However, soluble DNAM-1 binds to the fungal cell wall and blocking DNAM-1 reduces antifungal activity in colony-forming assays. Furthermore, in silico domain-domain interaction analysis identifies several fungal proteins as putative DNAM-1 targets, including OpsB in A. fumigatus and Sap10 in C. albicans. High-affinity binding between Sap10 and DNAM-1 is predicted computationally and confirmed experimentally by co-immunoprecipitation and fluorescence correlation spectroscopy. Microscopic analysis further demonstrates that Sap10 binds to primary NK cells but not to DNAM-1-deficient NK cells. Sap10 binding induced NK-cell activation, as evidenced by increased CD69 expression and elevated perforin and CCL3 secretion. These findings identify Sap10 as a fungal ligand of DNAM-1 and reveal a mechanism by which NK cells recognize fungal pathogens.
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