{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T04:45:43Z","timestamp":1790397943813,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,8,12]],"date-time":"2013-08-12T00:00:00Z","timestamp":1376265600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Activation of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells helps to establish and maintain immune responses. During infection with lymphocytic choriomeningitis virus (<jats:styled-content style=\"fixed-case\">LCMV<\/jats:styled-content>) clone 13, the <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T\u2010cell responses are lost. In this study, we were interested in the nature of the <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T\u2010cell responses following infection with <jats:styled-content style=\"fixed-case\">LCMV<\/jats:styled-content> clone 13. To pursue this question, we infected <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 mice with <jats:styled-content style=\"fixed-case\">LCMV<\/jats:styled-content> clone 13. We used a <jats:styled-content style=\"fixed-case\">GP<\/jats:styled-content>66\u201080 <jats:styled-content style=\"fixed-case\">MHC C<\/jats:styled-content>lass <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> tetramer to determine whether the <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells were present following infection with <jats:styled-content style=\"fixed-case\">LCMV<\/jats:styled-content> clone 13. We determined that the cells were present and antigen specific, but not functional. We attributed their dysfunction to the presence of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T\u2010cell inhibitory ligands. We further stained for the presence of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T\u2010cell inhibitory ligands. We found that the during chronic infection the number of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells expressing programmed death\u20101 and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>160 were greater over the time\u2013course study than the other <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T\u2010cell inhibitory ligands. These data show that using <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell inhibitory ligands as a reagent for characterization can help in understanding the complex immune responses associated with persistent infections.<\/jats:p>","DOI":"10.1111\/imm.12109","type":"journal-article","created":{"date-parts":[[2013,4,9]],"date-time":"2013-04-09T11:06:25Z","timestamp":1365505585000},"page":"61-69","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["<scp>CD<\/scp>4<sup>+<\/sup><scp>T<\/scp>\u2010cell inhibitory ligands: a tool for characterizing dysfunctional <scp>CD<\/scp>4<sup>+<\/sup> T cells during chronic infection"],"prefix":"10.1111","volume":"140","author":[{"given":"Courtney","family":"Dow","sequence":"first","affiliation":[{"name":"Department of Biological Sciences California State University 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