{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T00:10:24Z","timestamp":1771373424888,"version":"3.50.1"},"reference-count":20,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2014,1,13]],"date-time":"2014-01-13T00:00:00Z","timestamp":1389571200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"name":"Italian Telethon Foundation","award":["RF-2009-1485896"],"award-info":[{"award-number":["RF-2009-1485896"]}]},{"name":"Italian Telethon Foundation","award":["TIGET"],"award-info":[{"award-number":["TIGET"]}]},{"name":"Ministry of Health","award":["RF-2008-2009"],"award-info":[{"award-number":["RF-2008-2009"]}]},{"DOI":"10.13039\/501100005010","name":"Associazione Italiana per la Ricerca sul Cancro","doi-asserted-by":"crossref","award":["IG10157"],"award-info":[{"award-number":["IG10157"]}],"id":[{"id":"10.13039\/501100005010","id-type":"DOI","asserted-by":"crossref"}]},{"name":"EU Clinigene NoE","award":["LSHB-CT-2006-018933"],"award-info":[{"award-number":["LSHB-CT-2006-018933"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:p><jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>iskott\u2013<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>ldrich syndrome (<jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>) is a primary immunodeficiency caused by reduced or absent expression of the <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content> protein (<jats:styled-content style=\"fixed-case\">WASP<\/jats:styled-content>). <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content> patients are affected by microthrombocytopenia, recurrent infections, eczema, autoimmune diseases, and malignancies. Although immune deficiency has been proposed to play a role in tumor pathogenesis, there is little evidence on the correlation between immune cell defects and tumor susceptibility. Taking advantage of a tumor\u2010prone model, we show that the lack of <jats:styled-content style=\"fixed-case\">WASP<\/jats:styled-content> induces early tumor onset because of defective immune surveillance. Consistently, the <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>16 melanoma model shows that tumor growth and the number of lung metastases are increased in the absence of <jats:styled-content style=\"fixed-case\">WASP<\/jats:styled-content>. We then investigated the in vivo contribution of <jats:italic><jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>as<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells and <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s in controlling <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>16 melanoma development. We found fewer <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>16 metastases developed in the lungs of <jats:italic><jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>as<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice that had received <jats:styled-content style=\"fixed-case\">WT NK<\/jats:styled-content> cells as compared with mice bearing <jats:italic><jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>as<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells. Furthermore, we demonstrated that <jats:italic><jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>as<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s were less efficient in inducing <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content>\u2010cell activation in vitro and in vivo. In summary, for the first time, we demonstrate in in vivo models that <jats:styled-content style=\"fixed-case\">WASP<\/jats:styled-content> deficiency affects resistance to tumor and causes impairment in the antitumor capacity of <jats:styled-content style=\"fixed-case\">NK<\/jats:styled-content> cells and <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s.<\/jats:p>","DOI":"10.1002\/eji.201343935","type":"journal-article","created":{"date-parts":[[2013,12,13]],"date-time":"2013-12-13T18:32:57Z","timestamp":1386959577000},"page":"1039-1045","source":"Crossref","is-referenced-by-count":27,"title":["<scp>W<\/scp>iskott\u2013<scp>A<\/scp>ldrich syndrome protein deficiency in natural killer and dendritic cells affects antitumor immunity"],"prefix":"10.1002","volume":"44","author":[{"given":"Marco","family":"Catucci","sequence":"first","affiliation":[{"name":"TIGET, San Raffaele Scientific Institute  Milan 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