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Our aim was to better understand its role. We induced <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 in <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> of naive <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2\u2010deficient mice using intrathecally administered replication\u2010defective adenovirus and examined cell infiltration by flow cytometry. <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 expression induced pronounced and unexpected recruitment of regulatory and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u03b3\u2010producing T cells to <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> from blood, possibly related to defective egress of monocytes from <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2\u2010deficient bone marrow. Infiltration also occurred in mice lacking <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>2, a receptor for <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2. Expression of another receptor for <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2, <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>4, and <jats:styled-content style=\"fixed-case\">CXCR<\/jats:styled-content>3, a receptor for <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>10, which was also induced, were both increased in <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2\u2010treated <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>4 was expressed by neurons and astrocytes as well as <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4 T cells, and <jats:styled-content style=\"fixed-case\">CXCR<\/jats:styled-content>3 was expressed by <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4 and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8 T cells. Chemokine\u2010recruited T cells did not lead to <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> pathology. Our findings show a role for <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 in recruitment of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4 T cells to the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> and show that redundancy among chemokine receptors ensures optimal response.<\/jats:p>","DOI":"10.1111\/apm.12740","type":"journal-article","created":{"date-parts":[[2017,8,24]],"date-time":"2017-08-24T12:49:05Z","timestamp":1503578945000},"page":"945-956","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["<scp>CCL<\/scp>2 recruits T cells into the brain in a <scp>CCR<\/scp>2\u2010independent manner"],"prefix":"10.1111","volume":"125","author":[{"given":"Oriane","family":"C\u00e9dile","sequence":"first","affiliation":[{"name":"Department of Neurobiology Research Institute of Molecular Medicine University of Southern Denmark Odense 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