{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T23:08:40Z","timestamp":1792710520382,"version":"4.5.0"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2004,2,15]],"date-time":"2004-02-15T00:00:00Z","timestamp":1076803200000},"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":[[2004,2,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Chemokines are likely to play important roles in the pathophysiology of diseases associated with Epstein-Barr virus (EBV). Here, we have analyzed the repertoire of chemokines expressed by EBV-infected B cells. EBV infection of B cells induced expression of TARC\/CCL17 and MDC\/CCL22, which are known to attract Th2 cells and regulatory T cells via CCR4, and also upregulated constitutive expression of MIP-1\u03b1\/CCL3, MIP-1\u03b2\/CCL4, and RANTES\/CCL5, which are known to attract Th1 cells and cytotoxic T cells via CCR5. Accordingly, EBV-immortalized B cells secreted these chemokines, especially CCL3, CCL4, and CCL22, in large quantities. EBV infection or stable expression of LMP1 also induced CCL17 and CCL22 in a B-cell line, BJAB. The inhibitors of the TRAF\/NF-\u03baB pathway (BAY11-7082) and the p38\/ATF2 pathway (SB202190) selectively suppressed the expression of CCL17 and CCL22 in EBV-immortalized B cells and BJAB-LMP1. Consistently, transient-transfection assays using CCL22 promoter-reporter constructs demonstrated that two NF-\u03baB sites and a single AP-1 site were involved in the activation of the CCL22 promoter by LMP1. Finally, serum CCL22 levels were significantly elevated in infectious mononucleosis. Collectively, LMP1 induces CCL17 and CCL22 in EBV-infected B cells via activation of NF-\u03baB and probably ATF2. Production of CCL17 and CCL22, which attract Th2 and regulatory T cells, may help EBV-infected B cells evade immune surveillance by Th1 cells. However, the concomitant production of CCL3, CCL4, and CCL5 by EBV-infected B cells may eventually attract Th1 cells and cytotoxic T cells, leading to elimination of EBV-infected B cells at latency III and to selection of those with limited expression of latent genes.<\/jats:p>","DOI":"10.1128\/jvi.78.4.1665-1674.2004","type":"journal-article","created":{"date-parts":[[2004,1,27]],"date-time":"2004-01-27T19:58:01Z","timestamp":1075233481000},"page":"1665-1674","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":163,"title":["Selective Induction of Th2-Attracting Chemokines CCL17 and CCL22 in Human B Cells by Latent Membrane Protein 1 of Epstein-Barr Virus"],"prefix":"10.1128","volume":"78","author":[{"given":"Takashi","family":"Nakayama","sequence":"first","affiliation":[{"name":"Department of Microbiology, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kunio","family":"Hieshima","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daisuke","family":"Nagakubo","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emiko","family":"Sato","sequence":"additional","affiliation":[{"name":"Osaka Medical Center and Research Institute for Maternal and Child Health, Izumi City, Osaka 594-1101, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masahiro","family":"Nakayama","sequence":"additional","affiliation":[{"name":"Osaka Medical Center and Research Institute for Maternal and Child Health, Izumi City, Osaka 594-1101, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keisei","family":"Kawa","sequence":"additional","affiliation":[{"name":"Osaka Medical Center and Research Institute for Maternal and Child Health, Izumi City, Osaka 594-1101, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Osamu","family":"Yoshie","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri980"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V85.3.744.bloodjournal853744"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80622-6"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni735"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80623-8"},{"key":"e_1_3_2_7_2","first-page":"S5","volume":"9","year":"1998","unstructured":"Chapman, A. 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