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Here, we found that extracellular vesicles (EVs) derived from melanoma cells are rapidly transported by lymphatic vessels to draining LNs, where they selectively interact with lymphatic endothelial cells (LECs) as well as medullary sinus macrophages. Interestingly, uptake of melanoma EVs by LN\u2010resident LECs was partly dependent on lymphatic VCAM\u20101 expression, and induced transcriptional changes as well as proliferation of those cells. Furthermore, melanoma EVs shuttled tumour antigens to LN LECs for cross\u2010presentation on MHC\u2010I, resulting in apoptosis induction in antigen\u2010specific CD8<jats:sup>+<\/jats:sup> T cells. In conclusion, our data identify EV\u2010mediated melanoma\u2014LN LEC communication as a new pathway involved in tumour progression and tumour immune inhibition, suggesting that EV uptake or effector mechanisms in LECs might represent a new target for melanoma therapy.<\/jats:p>","DOI":"10.1002\/jev2.12197","type":"journal-article","created":{"date-parts":[[2022,2,21]],"date-time":"2022-02-21T07:42:49Z","timestamp":1645429369000},"source":"Crossref","is-referenced-by-count":133,"title":["Melanoma\u2010derived extracellular vesicles mediate lymphatic remodelling and impair tumour immunity in draining lymph nodes"],"prefix":"10.1002","volume":"11","author":[{"given":"Noelle","family":"Leary","sequence":"first","affiliation":[{"name":"Institute of Pharmaceutical Sciences Swiss Federal Institute of Technology (ETH) Zurich  Zurich Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarina","family":"Walser","sequence":"additional","affiliation":[{"name":"Institute 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