{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T03:42:22Z","timestamp":1790739742635,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,12,30]],"date-time":"2016-12-30T00:00:00Z","timestamp":1483056000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"NIHR Biomedical Research Centre"},{"name":"Bloodwise charity","award":["13060"],"award-info":[{"award-number":["13060"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Medicine"],"published-print":{"date-parts":[[2017,1]]},"abstract":"Abstract<\/jats:title>Adult T\u2010cell leukemia\/lymphoma (ATL<\/jats:styled-content>), a human T\u2010lymphotropic virus type 1 (HTLV<\/jats:styled-content>\u20101)\u2010associated disease, has a highly variable clinical course and four subtypes with therapeutic and prognostic implications. However, there are overlapping features between ATL<\/jats:styled-content> subtypes and between ATL<\/jats:styled-content> and nonmalignant (non\u2010ATL<\/jats:styled-content>) HTLV<\/jats:styled-content>\u20101 infection complicating diagnosis and prognostication. To further refine the diagnosis and prognosis of ATL<\/jats:styled-content>, we characterized the immunophenotype of HTLV<\/jats:styled-content>\u20101\u2010infected cells in ATL<\/jats:styled-content> and non\u2010ATL<\/jats:styled-content>. A retrospective study of peripheral blood samples from 10 HTLV<\/jats:styled-content>\u20101\u2010uninfected subjects (UI<\/jats:styled-content>), 54 HTLV<\/jats:styled-content>\u20101\u2010infected patients with non\u2010ATL<\/jats:styled-content>, and 22 with ATL<\/jats:styled-content> was performed using flow cytometry. All patients with ATL<\/jats:styled-content> had CD<\/jats:styled-content>4+<\/jats:sup>\u00a0CCR<\/jats:styled-content>4+<\/jats:sup>\u00a0CD<\/jats:styled-content>26\u2212<\/jats:sup> immunophenotype and the frequency of CD<\/jats:styled-content>4+<\/jats:sup>\u00a0CCR<\/jats:styled-content>4+<\/jats:sup>\u00a0CD<\/jats:styled-content>26\u2212<\/jats:sup> T cells correlated highly significantly with the proviral load in non\u2010ATL<\/jats:styled-content> suggesting CD<\/jats:styled-content>4+<\/jats:sup>\u00a0CCR<\/jats:styled-content>4+<\/jats:sup>\u00a0CD<\/jats:styled-content>26\u2212<\/jats:sup> as a marker of HTLV<\/jats:styled-content>\u20101\u2010infected cells. Further immunophenotyping of CD<\/jats:styled-content>4+<\/jats:sup>\u00a0CCR<\/jats:styled-content>4+<\/jats:sup>\u00a0 CD<\/jats:styled-content>26\u2212<\/jats:sup> cells revealed that 95% patients with ATL<\/jats:styled-content> had a CD<\/jats:styled-content>7\u2212<\/jats:sup> (\u226430% CD<\/jats:styled-content>7+<\/jats:sup> cells), whereas 95% HTLV<\/jats:styled-content>+ non\u2010ATL<\/jats:styled-content> had CD<\/jats:styled-content>7+<\/jats:sup> (>30% CD<\/jats:styled-content>7+<\/jats:sup> cells) immunophenotype. All patients with aggressive ATL<\/jats:styled-content> had a CCR<\/jats:styled-content>7+<\/jats:sup> (\u226530%), whereas 92% with indolent ATL<\/jats:styled-content> and 100% non\u2010ATL<\/jats:styled-content> had a CCR<\/jats:styled-content>7\u2212<\/jats:sup> (<30%) immunophenotype. Patients with nonprogressing indolent ATL<\/jats:styled-content> were CD<\/jats:styled-content>127+<\/jats:sup> but those with progressive lymphocytosis requiring systemic therapy had a CD<\/jats:styled-content>127\u2212<\/jats:sup> (\u226430%) immunophenotype. In summary, HTLV<\/jats:styled-content>\u20101\u2010infected cells have a CD<\/jats:styled-content>4+<\/jats:sup>\u00a0CCR<\/jats:styled-content>4+<\/jats:sup>\u00a0CD<\/jats:styled-content>26\u2212<\/jats:sup> immunophenotype. Within this population, CD<\/jats:styled-content>7\u2212<\/jats:sup> phenotype suggests a diagnosis of ATL<\/jats:styled-content>, CCR<\/jats:styled-content>7+<\/jats:sup> phenotype identifies aggressive ATL<\/jats:styled-content>, while CCR<\/jats:styled-content>7\u2212<\/jats:sup> CD<\/jats:styled-content>127\u2212<\/jats:sup> phenotype identifies progressive indolent ATL<\/jats:styled-content>.<\/jats:p>","DOI":"10.1002\/cam4.928","type":"journal-article","created":{"date-parts":[[2016,12,30]],"date-time":"2016-12-30T05:07:21Z","timestamp":1483074441000},"page":"298-309","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Risk stratification of adult T\u2010cell leukemia\/lymphoma using immunophenotyping"],"prefix":"10.1002","volume":"6","author":[{"given":"Huseini H.","family":"Kagdi","sequence":"first","affiliation":[{"name":"Section of Virology Department of Medicine Imperial College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria A.","family":"Demontis","sequence":"additional","affiliation":[{"name":"Section of Virology Department of Medicine Imperial College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul A.","family":"Fields","sequence":"additional","affiliation":[{"name":"Department of Hematology Guys Hospital London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan Carlos","family":"Ramos","sequence":"additional","affiliation":[{"name":"Department of Hematology\/Oncology University of Miami School of Medicine Miami Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles R. 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