{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T16:29:34Z","timestamp":1791044974153,"version":"4.1.0"},"reference-count":89,"publisher":"American Society of Hematology","issue":"4","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,8,15]]},"abstract":"<jats:p>Adult T-cell leukemia (ATL) is an aggressive malignancy of CD4+ T cells caused by the human T-cell leukemia virus type 1 (HTLV-1). The viral leukemogenesis is critically dependent on its oncoprotein Tax because the protein as well as the virus can immortalize primary human lymphocytes to permanent growth. As a transcriptional transactivator, Tax can stimulate the expression of distinct cellular genes. Alterations in the expression levels of unknown growth-relevant genes may contribute to the changed growth properties of Tax-immortalized and leukemic cells. To identify genes that are linked to Tax transformation and ATL leukemogenesis, this study systematically compared the gene expression of cultured cells from patients with acute ATL with that of stimulated peripheral blood T lymphocytes. Several overexpressed RNAs that encode signal transduction functions were identified. These include a dual-specific protein phosphatase (PAC1), an interferon-inducible factor (ISG15), a basic helix-loop-helix transcription factor (DEC-1), and the secreted antiapoptotic chemokine I-309. The ATL cell culture supernatants contained an antiapoptotic activity that could be specifically inhibited by antibodies directed against I-309. Inhibition of I-309 receptor (CCR8) signaling by pertussis toxin increased the apoptosis rate of ATL cell cultures in the presence and absence of external apoptotic stimuli. Both the I-309\u2013specific antiapoptotic activity and the proapoptotic effect of inhibitors of I-309 signaling suggest the existence of an antiapoptotic autocrine loop in ATL cells. Thus, the overexpression of this chemokine may inhibit apoptosis in ATL cells and could substantially contribute to their growth.<\/jats:p>","DOI":"10.1182\/blood.v98.4.1150","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T12:46:47Z","timestamp":1027774007000},"page":"1150-1159","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":100,"title":["Autocrine antiapoptotic stimulation of cultured adult T-cell leukemia cells by overexpression of the chemokine I-309"],"prefix":"10.1182","volume":"98","author":[{"given":"Tobias","family":"Ruckes","sequence":"first","affiliation":[{"name":"From the Institut fu\u0308r Klinische und Molekulare Virologie, Erlangen, Germany; Ludwig Institute for Cancer Research, Brussels Branch, Universite\u0301 Catholique de Louvain, Belgium; and Department of Clinical Hematology, Ho\u0302pital Necker, Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Domenica","family":"Saul","sequence":"additional","affiliation":[{"name":"From the Institut fu\u0308r Klinische und Molekulare Virologie, Erlangen, Germany; Ludwig Institute for Cancer Research, Brussels Branch, Universite\u0301 Catholique de Louvain, Belgium; and Department of Clinical Hematology, Ho\u0302pital Necker, Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacques","family":"Van Snick","sequence":"additional","affiliation":[{"name":"From the Institut fu\u0308r Klinische und Molekulare Virologie, Erlangen, Germany; Ludwig Institute for Cancer Research, Brussels Branch, Universite\u0301 Catholique de Louvain, Belgium; and Department of Clinical Hematology, Ho\u0302pital Necker, Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivier","family":"Hermine","sequence":"additional","affiliation":[{"name":"From the Institut fu\u0308r Klinische und 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