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Notably, DC roles in regulating innate CD11b<jats:sup>+<\/jats:sup>Ly-6C<jats:sup>hi<\/jats:sup> monocyte functions during neuroinflammation have not yet been addressed. Using selective ablation of CD11c<jats:sup>hi<\/jats:sup>PDCA-1<jats:sup>int\/lo<\/jats:sup> DCs without alteration in CD11c<jats:sup>int<\/jats:sup>PDCA-1<jats:sup>hi<\/jats:sup> plasmacytoid DC number, we found that CD11c<jats:sup>hi<\/jats:sup> DCs are essential to control neuroinflammation caused by infection with neurotropic Japanese encephalitis virus, through early and increased infiltration of CD11b<jats:sup>+<\/jats:sup>Ly-6C<jats:sup>hi<\/jats:sup> monocytes and higher expression of CC chemokines. More interestingly, selective CD11c<jats:sup>hi<\/jats:sup> DC ablation provided altered differentiation and function of infiltrated CD11b<jats:sup>+<\/jats:sup>Ly-6C<jats:sup>hi<\/jats:sup> monocytes in the CNS through Flt3-L and GM-CSF, which was closely associated with severely enhanced neuroinflammation. Furthermore, CD11b<jats:sup>+<\/jats:sup>Ly-6C<jats:sup>hi<\/jats:sup> monocytes generated in CD11c<jats:sup>hi<\/jats:sup> DC-ablated environment had a deleterious rather than protective role during neuroinflammation and were more quickly recruited into inflamed CNS, depending on CCR2, thereby exacerbating neuroinflammation <jats:italic>via<\/jats:italic> enhanced supply of virus from the periphery. Therefore, our data demonstrate that CD11c<jats:sup>hi<\/jats:sup> DCs provide a critical and unexpected role to preserve the immune-privileged CNS in lethal neuroinflammation <jats:italic>via<\/jats:italic> regulating the differentiation, function and trafficking of CD11b<jats:sup>+<\/jats:sup>Ly-6C<jats:sup>hi<\/jats:sup> monocytes.<\/jats:p>","DOI":"10.1038\/srep17548","type":"journal-article","created":{"date-parts":[[2015,12,2]],"date-time":"2015-12-02T10:03:13Z","timestamp":1449050593000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["CD11chi Dendritic Cells Regulate Ly-6Chi Monocyte Differentiation to Preserve Immune-privileged CNS in Lethal Neuroinflammation"],"prefix":"10.1038","volume":"5","author":[{"given":"Jin Hyoung","family":"Kim","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jin Young","family":"Choi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seong Bum","family":"Kim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erdenebelig","family":"Uyangaa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ajit Mahadev","family":"Patil","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Young Woo","family":"Han","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sang-Youel","family":"Park","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John Hwa","family":"Lee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Koanhoi","family":"Kim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seong Kug","family":"Eo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2015,12,2]]},"reference":[{"key":"BFsrep17548_CR1","doi-asserted-by":"publisher","first-page":"1164","DOI":"10.1172\/JCI58644","volume":"122","author":"RM Ransohoff","year":"2012","unstructured":"Ransohoff, R. 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