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This study investigated the role of fungal EVs in both intra- and interspecies communication, focusing on their effects on virulence and immune responses. Co-incubation experiments were performed using EVs derived from\n                      <jats:italic toggle=\"yes\">Candida albicans<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Candidozyma auris<\/jats:italic>\n                      to assess interactions with\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      planktonic cells and biofilms, as well as\n                      <jats:italic toggle=\"yes\">Cryptococcus neoformans<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Cryptococcus gattii<\/jats:italic>\n                      EVs interacting with\n                      <jats:italic toggle=\"yes\">C. neoformans<\/jats:italic>\n                      cultures. EVs were observed associating with recipient cell surfaces, suggesting subsequent internalization. Functional assays revealed that EV exposure led to increased expression of\n                      <jats:italic toggle=\"yes\">CAP59, LAC1, URE1,<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">ERG11<\/jats:italic>\n                      genes, correlating with reduced antifungal susceptibility in both planktonic and biofilm forms. Additionally, EVs facilitated cross-species communication, enhancing biofilm adhesion and dispersion, which emphasizes their role in phenotypic modulation. Macrophages stimulated with fungal EVs exhibited receptor-specific gene expression changes (dependent on the EVs\u2019 origin, including variation among species of the same genus), along with a pro-inflammatory phenotype marked by increased\n                      <jats:italic toggle=\"yes\">iNOS<\/jats:italic>\n                      expression, enhanced TBK1\/STAT1 production, and elevated levels of IL-1\u03b2, IL-6, and IL-8. Collectively, these findings underscore a critical role for fungal EVs in interspecies communication, biofilm regulation, and immune modulation, offering valuable insights into fungal pathogenicity mechanisms.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>Currently, no vaccines exist to prevent fungal infections, underscoring the need for new therapies. As fungal diseases increase globally, understanding fungal biology is essential to identifying treatment targets. Fungi use extracellular vesicles (EVs) to communicate and evade immune responses. EVs mediate cell-cell communication, transporting proteins, polysaccharides, lipids, and nucleic acids, serving as \u201cmessages\u201d exchanged within a fungal network. Understanding how these vesicles facilitate communication not only within a single species but also across different fungal species can shed light on their contribution to infection persistence and cross-species adaptability. Moreover, EVs may have a broader role in inter-kingdom signaling, influencing how fungi interact with host immune cells. The impact of fungal EVs on human innate immune responses remains a largely underexplored area, with significant gaps in our knowledge. This study aims to examine how fungal EVs affect immune responses and whether their signaling varies across species, potentially revealing new therapeutic targets.<\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.03469-25","type":"journal-article","created":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T14:00:33Z","timestamp":1769781633000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":7,"title":["Fungal extracellular vesicles mediate conserved cross-species communication and immunomodulation"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6650-8286","authenticated-orcid":false,"given":"Renan E. 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