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Here we show that this evasion is independent of known immune\u2010escape traits of\n                    <jats:italic>C. albicans<\/jats:italic>\n                    . Instead, neutrophil\u2010derived extracellular vesicles (EVs) enriched in antimicrobial proteins and neutrophil surface markers (CD66b, CD45, CD63, and complement receptors CR1, CR3 and CR4) promote this state. Isolated EVs bound to\n                    <jats:italic>C. albicans<\/jats:italic>\n                    preferentially in a complement\u2010dependent manner, and this binding was partially inhibited by anti\u2010CD11b, supporting CR3 involvement. Despite their antimicrobial cargo, EVs did not impair fungal growth. Instead, EV coating reduced neutrophil phagocytosis in purified\u2010cell and whole\u2010blood settings. These findings reveal a dual role for neutrophil\u2010derived EVs at the host\u2010pathogen interface: although enriched for innate effector molecules with potential antifungal activity, their deposition on\n                    <jats:italic>C. albicans<\/jats:italic>\n                    does not impair growth but is associated with reduced phagocytosis and maintenance of an extracellular population.\n                  <\/jats:p>","DOI":"10.1002\/jev2.70363","type":"journal-article","created":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T18:36:01Z","timestamp":1788028561000},"source":"Crossref","is-referenced-by-count":0,"title":["Host\u2010to\u2010Pathogen Transfer of Neutrophil Components via Extracellular Vesicles Shields\n                    <i>Candida albicans<\/i>\n                    From Immune Attack in Human Blood"],"prefix":"10.1002","volume":"15","author":[{"given":"Jennifer J.","family":"Patitz","sequence":"first","affiliation":[{"name":"Institute for Hygiene and 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