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Here we found that, compared with peripheral blood T cells, tumor-infiltrating T cells contained a higher frequency of effector Tregs, which are defined as FOXP3\n                    <jats:sup>hi<\/jats:sup>\n                    and CD45RA\n                    <jats:sup>\u2212<\/jats:sup>\n                    , terminally differentiated, and most suppressive. Effector Treg cells, but not FOXP3\n                    <jats:sup>lo<\/jats:sup>\n                    and CD45RA\n                    <jats:sup>+<\/jats:sup>\n                    na\u00efve Treg cells, predominantly expressed C-C chemokine receptor 4 (CCR4) in both cancer tissues and peripheral blood. In vivo or in vitro anti-CCR4 mAb treatment selectively depleted effector Treg cells and efficiently induced tumor-antigen-specific CD4\n                    <jats:sup>+<\/jats:sup>\n                    and CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells. Thus, cell-depleting anti-CCR4 mAb therapy is instrumental for evoking and enhancing tumor immunity in humans via selectively removing effector-type FOXP3\n                    <jats:sup>+<\/jats:sup>\n                    Treg cells.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1316796110","type":"journal-article","created":{"date-parts":[[2013,10,14]],"date-time":"2013-10-14T20:21:48Z","timestamp":1381782108000},"page":"17945-17950","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":610,"title":["Anti-CCR4 mAb selectively depletes effector-type FoxP3\n                    <sup>+<\/sup>\n                    CD4\n                    <sup>+<\/sup>\n                    regulatory T cells, evoking antitumor immune responses in humans"],"prefix":"10.1073","volume":"110","author":[{"given":"Daisuke","family":"Sugiyama","sequence":"first","affiliation":[{"name":"Experimental Immunology, World Premier International Research Center, Immunology Frontier Research Center,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroyoshi","family":"Nishikawa","sequence":"additional","affiliation":[{"name":"Experimental Immunology, World Premier International Research Center, Immunology Frontier Research Center,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuka","family":"Maeda","sequence":"additional","affiliation":[{"name":"Experimental Immunology, World Premier International Research Center, Immunology Frontier Research Center,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megumi","family":"Nishioka","sequence":"additional","affiliation":[{"name":"Experimental Immunology, World Premier International Research Center, Immunology Frontier Research Center,"},{"name":"Department of Dermatology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atsushi","family":"Tanemura","sequence":"additional","affiliation":[{"name":"Department of Dermatology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ichiro","family":"Katayama","sequence":"additional","affiliation":[{"name":"Department of Dermatology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sachiko","family":"Ezoe","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuzuru","family":"Kanakura","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eiichi","family":"Sato","sequence":"additional","affiliation":[{"name":"Department of Anatomic Pathology, Tokyo Medical University, Tokyo 160-8402, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuo","family":"Fukumori","sequence":"additional","affiliation":[{"name":"The Third Section of Clinical Investigation, Kinki Blood Center, Osaka 536-8505, Japan; 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