{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:40:58Z","timestamp":1786977658413,"version":"build-2736575974"},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,1,13]],"date-time":"2014-01-13T00:00:00Z","timestamp":1389571200000},"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":[[2014,3]]},"abstract":"<jats:p>\n                    Most differentiated\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    8\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    cells die off at the end of an infection, revealing two main subsets of memory T cells \u2014 central and effector memory \u2014 which can be found in lymphoid tissues or circulating through nonlymphoid organs, respectively. The cell intrinsic regulation of the differentiation of\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    8\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    cells to effector and central memory remains poorly studied. Herein, we describe a novel role of the\n                    <jats:styled-content style=\"fixed-case\">ETS<\/jats:styled-content>\n                    transcription factor\n                    <jats:styled-content style=\"fixed-case\">ELF<\/jats:styled-content>\n                    4 in the development and function of memory\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    8\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    cells following infection with\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>\n                      isteria monocytogenes\n                    <\/jats:italic>\n                    . Adoptively transferred\n                    <jats:italic>\n                      Elf4\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    na\u00efve\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    8\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    cells produced lower numbers of effector memory\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    8\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    cells despite a normal pool of central memory. This was caused by suboptimal priming and decreased survival of\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    8\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    cells at the peak of response while enhanced\n                    <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                    otch1 signaling and upregulation of eomesodermin correlated with \u201cnormal\u201d development of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\n                      lf4\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    central memory. Finally, loss of\n                    <jats:styled-content style=\"fixed-case\">ELF<\/jats:styled-content>\n                    4 impaired the expansion of both central and effector memory\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    8\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    cells in a recall response by also activating\n                    <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                    otch1 signaling. Altogether,\n                    <jats:styled-content style=\"fixed-case\">ELF<\/jats:styled-content>\n                    4 emerges as a novel transcriptional regulator of\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    8\n                    <jats:sup>+<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    \u2010cell differentiation in response to infection.\n                  <\/jats:p>","DOI":"10.1002\/eji.201343775","type":"journal-article","created":{"date-parts":[[2013,12,13]],"date-time":"2013-12-13T19:22:42Z","timestamp":1386962562000},"page":"715-727","source":"Crossref","is-referenced-by-count":15,"title":["Transcription factor\n                    <scp>ELF<\/scp>\n                    4 promotes development and function of memory\n                    <scp>CD<\/scp>\n                    8\n                    <sup>+<\/sup>\n                    <scp>T<\/scp>\n                    cells in\n                    <i>\n                      <scp>L<\/scp>\n                      isteria monocytogenes\n                    <\/i>\n                    infection"],"prefix":"10.1002","volume":"44","author":[{"given":"Maksim","family":"Mamonkin","sequence":"first","affiliation":[{"name":"Department of Pathology &amp; Immunology Baylor College of Medicine Texas Children's Hospital  Houston TX USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monica","family":"Puppi","sequence":"additional","affiliation":[{"name":"Department of Pathology &amp; Immunology Baylor College of Medicine Texas Children's Hospital  Houston TX USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. 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