{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T13:21:36Z","timestamp":1792156896600,"version":"4.4.0"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"19","license":[{"start":{"date-parts":[[2017,10,1]],"date-time":"2017-10-01T00:00:00Z","timestamp":1506816000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2017,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            We previously reported that the T-cell receptor (TCR) repertoire of human T-cell lymphotropic virus type 1 (HTLV-1) Tax\n            <jats:sub>301-309<\/jats:sub>\n            -specific CD8\n            <jats:sup>+<\/jats:sup>\n            cytotoxic T cells (Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs) was highly restricted and a particular amino acid sequence motif, the PDR motif, was conserved among HLA-A*24:02-positive (HLA-A*24:02\n            <jats:sup>+<\/jats:sup>\n            ) adult T-cell leukemia\/lymphoma (ATL) patients who had undergone allogeneic hematopoietic cell transplantation (allo-HSCT). Furthermore, we found that donor-derived PDR\n            <jats:sup>+<\/jats:sup>\n            CTLs selectively expanded in ATL long-term HSCT survivors with strong CTL activity against HTLV-1. On the other hand, the TCR repertoires in Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs of asymptomatic HTLV-1 carriers (ACs) remain unclear. In this study, we directly identified the DNA sequence of complementarity-determining region 3 (CDR3) of the TCR-\u03b2 chain of Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs at the single-cell level and compared not only the TCR repertoires but also the frequencies and phenotypes of Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs between ACs and ATL patients. We did not observe any essential difference in the frequencies of Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs between ACs and ATL patients. In the single-cell TCR repertoire analysis of Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs, 1,458 Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs and 140 clones were identified in this cohort. Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs showed highly restricted TCR repertoires with a strongly biased usage of BV7, and PDR, the unique motif in TCR-\u03b2 CDR3, was exclusively observed in all ACs and ATL patients. However, there was no correlation between PDR\n            <jats:sup>+<\/jats:sup>\n            CTL frequencies and HTLV-1 proviral load (PVL). In conclusion, we have identified, for the first time, a unique amino acid sequence, PDR, as a public TCR-CDR3 motif against Tax in HLA-A*24:02\n            <jats:sup>+<\/jats:sup>\n            HTLV-1-infected individuals. Further investigations are warranted to elucidate the role of the PDR\n            <jats:sup>+<\/jats:sup>\n            CTL response in the progression from carrier state to ATL.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            ATL is an aggressive T-cell malignancy caused by HTLV-1 infection. The HTLV-1 regulatory protein Tax aggressively promotes the proliferation of HTLV-1-infected lymphocytes and is also a major target antigen for CD8\n            <jats:sup>+<\/jats:sup>\n            CTLs. In our previous evaluation of Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs, we found that a unique amino acid sequence motif, PDR, in CDR3 of the TCR-\u03b2 chain of Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs was conserved among ATL patients after allo-HSCT. Furthermore, the PDR\n            <jats:sup>+<\/jats:sup>\n            Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTL clones selectively expanded and showed strong cytotoxic activities against HTLV-1. On the other hand, it remains unclear how Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTL repertoire exists in ACs. In this study, we comprehensively compared Tax-specific TCR repertoires at the single-cell level between ACs and ATL patients. Tax\n            <jats:sub>301-309<\/jats:sub>\n            -CTLs showed highly restricted TCR repertoires with a strongly biased usage of BV7, and PDR, the unique motif in TCR-\u03b2 CDR3, was conserved in all ACs and ATL patients, regardless of clinical subtype in HTLV-1 infection.\n          <\/jats:p>","DOI":"10.1128\/jvi.00974-17","type":"journal-article","created":{"date-parts":[[2017,7,20]],"date-time":"2017-07-20T00:50:22Z","timestamp":1500511822000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":15,"title":["A Unique T-Cell Receptor Amino Acid Sequence Selected by Human T-Cell Lymphotropic Virus Type 1 Tax\n            <sub>301-309<\/sub>\n            -Specific Cytotoxic T Cells in HLA-A24:02-Positive Asymptomatic Carriers and Adult T-Cell Leukemia\/Lymphoma Patients"],"prefix":"10.1128","volume":"91","author":[{"given":"Yuko","family":"Ishihara","sequence":"first","affiliation":[{"name":"Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yukie","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, Japan"},{"name":"Division of Molecular Therapy, Institute of Medical Science, The University of Tokyo, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seiichiro","family":"Kobayashi","sequence":"additional","affiliation":[{"name":"Division of Molecular Therapy, Institute of Medical Science, The University of Tokyo, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koji","family":"Kawamura","sequence":"additional","affiliation":[{"name":"Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideki","family":"Nakasone","sequence":"additional","affiliation":[{"name":"Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayumi","family":"Gomyo","sequence":"additional","affiliation":[{"name":"Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jin","family":"Hayakawa","sequence":"additional","affiliation":[{"name":"Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaharu","family":"Tamaki","sequence":"additional","affiliation":[{"name":"Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, 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