{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T06:16:11Z","timestamp":1791353771920,"version":"4.3.1"},"reference-count":24,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,7,17]],"date-time":"2012-07-17T00:00:00Z","timestamp":1342483200000},"content-version":"vor","delay-in-days":16,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2012,7]]},"abstract":"<jats:p>Chronic myeloid leukemia (<jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>) is a clonal hematopoietic stem\u2010cell malignancy characterized by the presence of the chimeric <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ABL<\/jats:styled-content> oncoprotein with deregulated tyrosine\u2010kinase (<jats:styled-content style=\"fixed-case\">TK<\/jats:styled-content>) activity. Although conventional <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells are acknowledged as important players in the control of <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>, a possible modification of invariant <jats:styled-content style=\"fixed-case\">NKT<\/jats:styled-content> (i<jats:styled-content style=\"fixed-case\">NKT<\/jats:styled-content>) cells, known for their antitumoral activity, has not been established as yet. Here, we showed that the expression of perforin, <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>95<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>, and promyelocytic leukemia zinc finger, a transcription factor required for maintenance of i<jats:styled-content style=\"fixed-case\">NKT<\/jats:styled-content> cell functions, was reduced or suppressed in <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients at diagnosis, as compared with healthy individuals. The proliferation rate of blood i<jats:styled-content style=\"fixed-case\">NKT<\/jats:styled-content> cells in response to their cognate ligand was likewise diminished. These functional deficiencies were corrected in patients having achieved complete cytogenetic remission following <jats:styled-content style=\"fixed-case\">TK<\/jats:styled-content> inhibitor or <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b1 therapy. i<jats:styled-content style=\"fixed-case\">NKT<\/jats:styled-content> cells from <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients in the chronic phase did not display increased <jats:styled-content style=\"fixed-case\">TK<\/jats:styled-content> activity, which argued against a direct autonomous action of <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ABL<\/jats:styled-content>. Instead, we found that their anergic status originated from both intrinsic and <jats:styled-content style=\"fixed-case\">APC<\/jats:styled-content>\u2010dependent dysfunctions. Our data demonstrate that chronic phase <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> is associated with functional deficiencies of i<jats:styled-content style=\"fixed-case\">NKT<\/jats:styled-content> cells that are restored upon remission. These results suggest a possible contribution to disease control by <jats:styled-content style=\"fixed-case\">TK<\/jats:styled-content> inhibitor therapies.<\/jats:p>","DOI":"10.1002\/eji.201142043","type":"journal-article","created":{"date-parts":[[2012,5,14]],"date-time":"2012-05-14T12:46:15Z","timestamp":1336999575000},"page":"1870-1875","source":"Crossref","is-referenced-by-count":26,"title":["Evidence for <scp>BCR<\/scp>\u2010<scp>ABL<\/scp>\u2010dependent dysfunctions of i<scp>NKT<\/scp> cells from chronic myeloid leukemia patients"],"prefix":"10.1002","volume":"42","author":[{"given":"Alexis","family":"Rossignol","sequence":"first","affiliation":[{"name":"INSERM UMR S935  Poitiers and Villejuif France"},{"name":"Universit\u00e9 de Poitiers  Poitiers France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana\u00efs","family":"Levescot","sequence":"additional","affiliation":[{"name":"INSERM UMR S935  Poitiers and Villejuif France"},{"name":"Universit\u00e9 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