{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T17:10:43Z","timestamp":1790788243389,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2013,6,12]],"date-time":"2013-06-12T00:00:00Z","timestamp":1370995200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:p>We show here that the expression of 4\u20131<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> is rapidly induced in \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells following antigenic stimulation in both mice and humans, and ligation of the newly acquired 4\u20131<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> with an agonistic anti\u20104\u20131<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> augments cell division and cytokine production. We further demonstrate that \u03b3\u03b4 rather than \u03b1\u03b2 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells protect mice from <jats:italic><jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>isteria monocytogenes<\/jats:italic> (<jats:styled-content style=\"fixed-case\">LM<\/jats:styled-content>) infection and 4\u20131<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> stimulation enhances the \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell activities in the acute phase of <jats:styled-content style=\"fixed-case\">LM<\/jats:styled-content> infection. <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 produced from \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells was the major soluble factor regulating <jats:styled-content style=\"fixed-case\">LM<\/jats:styled-content> infection. <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\u03b31<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells were expanded in <jats:styled-content style=\"fixed-case\">LM<\/jats:styled-content>\u2010infected mice and 4\u20131<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> signal triggered an exclusive expansion of <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\u03b31<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells and induced <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 in these <jats:styled-content style=\"fixed-case\">V<\/jats:styled-content>\u03b31<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells. Similarly, 4\u20131<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> was induced on human \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells and shown to be fully functional. Combination treatment with human \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells and anti\u2010hu4\u20131<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> effectively protected against <jats:styled-content style=\"fixed-case\">LM<\/jats:styled-content> infection in human \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cell\u2010transferred <jats:styled-content style=\"fixed-case\">NOD<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">SCID<\/jats:styled-content> mice. Taken together, these data provide evidence that the 4\u20131<jats:styled-content style=\"fixed-case\">BB<\/jats:styled-content> signal is an important regulator of \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells and induces robust host defense against <jats:styled-content style=\"fixed-case\">LM<\/jats:styled-content> infection.<\/jats:p>","DOI":"10.1002\/eji.201242842","type":"journal-article","created":{"date-parts":[[2013,5,3]],"date-time":"2013-05-03T10:47:15Z","timestamp":1367578035000},"page":"1839-1848","source":"Crossref","is-referenced-by-count":34,"title":["4\u20131<scp>BB<\/scp> signal stimulates the activation, expansion, and effector functions of \u03b3\u03b4 <scp>T<\/scp> cells in mice and humans"],"prefix":"10.1002","volume":"43","author":[{"given":"Seung J.","family":"Lee","sequence":"first","affiliation":[{"name":"Immune &amp; Cell Therapy Branch National Cancer Center  Ilsan Gyeonggi\u2010do Korea"},{"name":"Department of Biological Sciences University of Ulsan  Ulsan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young H.","family":"Kim","sequence":"additional","affiliation":[{"name":"Immune &amp; Cell Therapy Branch National Cancer Center  Ilsan Gyeonggi\u2010do Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sun H.","family":"Hwang","sequence":"additional","affiliation":[{"name":"Immune &amp; Cell Therapy Branch National Cancer Center  Ilsan Gyeonggi\u2010do Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu. 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