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A persistent\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    infection is characterized by a lack of or a weak\n                    <jats:styled-content style=\"fixed-case\">CTL<\/jats:styled-content>\n                    response to\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    , which may be reflective of tolerance to\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    . Efficient induction of\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    \u2010specific\n                    <jats:styled-content style=\"fixed-case\">CTL<\/jats:styled-content>\n                    s leads to the clearance of\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    in patients with a chronic\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    infection. Previously, we reported that\n                    <jats:italic>\u03b1<\/jats:italic>\n                    \u2010galactosylceramide (\n                    <jats:italic>\u03b1<\/jats:italic>\n                    \u2010GalCer), a specific natural killer T (\n                    <jats:styled-content style=\"fixed-case\">NKT<\/jats:styled-content>\n                    ) cell agonist, enhanced the induction of\n                    <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\n                    surface antigen (\n                    <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\n                    sAg)\u2010specific\n                    <jats:styled-content style=\"fixed-case\">CTL<\/jats:styled-content>\n                    s. In the present study, we found that inhibition of indoleamine 2,3\u2010dioxygenase (\n                    <jats:styled-content style=\"fixed-case\">IDO<\/jats:styled-content>\n                    ) activity enhanced the induction of\n                    <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\n                    sAg\u2010specific\n                    <jats:styled-content style=\"fixed-case\">CTL<\/jats:styled-content>\n                    s after immunization with\n                    <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\n                    sAg and\n                    <jats:italic>\u03b1<\/jats:italic>\n                    \u2010GalCer. The administration of\n                    <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\n                    sAg and\n                    <jats:italic>\u03b1<\/jats:italic>\n                    \u2010GalCer increased the production of interleukin\u20102 and interleukin\u201012b, which are crucial for the induction of\n                    <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\n                    sAg\u2010specific\n                    <jats:styled-content style=\"fixed-case\">CTL<\/jats:styled-content>\n                    s. The production of these cytokines was more strongly enhanced in\n                    <jats:styled-content style=\"fixed-case\">IDO<\/jats:styled-content>\n                    knockout mice compared with wild\u2010type mice. In addition,\n                    <jats:italic>\u03b1<\/jats:italic>\n                    \u2010GalCer induced the production of\n                    <jats:styled-content style=\"fixed-case\">IDO<\/jats:styled-content>\n                    in\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    11b\n                    <jats:sup>+<\/jats:sup>\n                    cells, and these cells inhibited proliferation of\n                    <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\n                    sAg\u2010specific\n                    <jats:styled-content style=\"fixed-case\">CTL<\/jats:styled-content>\n                    s. Our results lead to strategies for improving the induction of\n                    <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\n                    sAg\u2010specific\n                    <jats:styled-content style=\"fixed-case\">CTL<\/jats:styled-content>\n                    s.\n                  <\/jats:p>","DOI":"10.1111\/imm.12274","type":"journal-article","created":{"date-parts":[[2014,3,3]],"date-time":"2014-03-03T05:54:55Z","timestamp":1393826095000},"page":"614-623","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Induction of hepatitis B virus surface antigen\u2010specific cytotoxic\n                    <scp>T<\/scp>\n                    lymphocytes can be up\u2010regulated by the inhibition of indoleamine 2, 3\u2010dioxygenase activity"],"prefix":"10.1111","volume":"142","author":[{"given":"Hiroyasu","family":"Ito","sequence":"first","affiliation":[{"name":"Department of 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