{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T01:44:30Z","timestamp":1792028670245,"version":"4.4.0"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2010,7,1]],"date-time":"2010-07-01T00:00:00Z","timestamp":1277942400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>We recently reported that human T-lymphotropic virus type 1 (HTLV-1) infection is accompanied by a high frequency of CD4+FoxP3+ cells in the circulation. In asymptomatic carriers of HTLV-1 and in patients with HTLV-1\u2013associated inflammatory and malignant diseases, a high FoxP3+ cell frequency correlated with inefficient cytotoxic T cell-mediated killing of HTLV-1\u2013infected cells. In adult T cell leukemia\/lymphoma (ATLL), the FoxP3+ population was distinct from the leukemic T cell clones. However, the cause of the increase in FoxP3+ cell frequency in HTLV-1 infection was unknown. In this study, we report that the plasma concentration of the chemokine CCL22 is abnormally high in HTLV-1\u2013infected subjects and that the concentration is strongly correlated with the frequency of FoxP3+ cells, which express the CCL22 receptor CCR4. Further, we show that CCL22 is produced by cells that express the HTLV-1 transactivator protein Tax, and that the increased CCL22 enhances the migration and survival of FoxP3+ cells in vitro. Finally, we show that FoxP3+ cells inhibit the proliferation of ex vivo, autologous leukemic clones from patients with ATLL. We conclude that HTLV-1\u2013induced CCL22 causes the high frequency of FoxP3+ cells observed in HTLV-1 infection; these FoxP3+ cells may both retard the progression of ATLL and HTLV-1\u2013associated inflammatory diseases and contribute to the immune suppression seen in HTLV-1 infection, especially in ATLL.<\/jats:p>","DOI":"10.4049\/jimmunol.0903846","type":"journal-article","created":{"date-parts":[[2010,6,5]],"date-time":"2010-06-05T02:41:27Z","timestamp":1275705687000},"page":"183-189","source":"Crossref","is-referenced-by-count":71,"title":["Human T-Lymphotropic Virus Type 1-Induced CC Chemokine Ligand 22 Maintains a High Frequency of Functional FoxP3+ Regulatory T Cells"],"prefix":"10.1093","volume":"185","author":[{"given":"Frederic","family":"Toulza","sequence":"first","affiliation":[{"name":"Department of Immunology, Imperial College , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kisato","family":"Nosaka","sequence":"additional","affiliation":[{"name":"Department of Hematology, Kumamoto University School of Medicine , Kumamoto ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuetsu","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Graduate School and Faculty of Medicine, University of the Ryukyus , Okinawa ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiziana","family":"Schioppa","sequence":"additional","affiliation":[{"name":"Centre for Cancer and Inflammation, Institute of Cancer, Barts and The London School of Medicine and Dentistry , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frances","family":"Balkwill","sequence":"additional","affiliation":[{"name":"Centre for Cancer and Inflammation, Institute of Cancer, Barts and The London School of Medicine and Dentistry , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Graham P","family":"Taylor","sequence":"additional","affiliation":[{"name":"Department of Genito-Urinary Medicine, Imperial College , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles R M","family":"Bangham","sequence":"additional","affiliation":[{"name":"Department of Immunology, Imperial College , London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2010,7,1]]},"reference":[{"key":"2025032411364189300_r1","doi-asserted-by":"crossref","first-page":"1031","DOI":"10.1016\/S0140-6736(86)91298-5","article-title":"HTLV-I associated myelopathy, a new clinical entity","volume":"1","author":"Osame","year":"1986","journal-title":"Lancet"},{"key":"2025032411364189300_r2","doi-asserted-by":"crossref","first-page":"228","DOI":"10.1080\/13550280390194028","article-title":"Human T-cell lymphotropic virus type I and neurological diseases","volume":"9","author":"Nagai","year":"2003","journal-title":"J. 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