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Here, we show that low\u2010dose infection with lymphocytic choriomeningitis virus (LCMV) caused rapid, transient inflammatory monocytosis that required type I interferon (IFN) and Toll\u2010like receptor (TLR) 7 signaling. Type I IFN and TLR7 signals were critical for induction of IFN\u2010stimulated gene expression and CCR2 ligand upregulation in the BM microenvironment in response to LCMV infection. Experiments utilizing BM chimeric mice demonstrated that type I IFN and TLR7 signaling on either hematopoietic or nonhematopoietic cells was sufficient to initiate monocytosis in response to LCMV infection. BM plasmacytoid dendritic cells (pDCs) generated type I IFN directly ex vivo, suggesting that pDCs are a hematopoietic contributor of type I IFN in the BM early during LCMV infection. Overall, we describe novel roles for type I IFN and TLR7 signaling in nonhematopoietic cells and BM pDCs in directing IFN\u2010stimulated gene and CCR2 ligand expression in the BM to initiate an increase in blood inflammatory monocytes during viral infection.<\/jats:p>","DOI":"10.1002\/eji.201445331","type":"journal-article","created":{"date-parts":[[2015,8,20]],"date-time":"2015-08-20T02:54:00Z","timestamp":1440039240000},"page":"3064-3072","source":"Crossref","is-referenced-by-count":4,"title":["Hematopoietic and nonhematopoietic cells promote Type I interferon\u2010 and TLR7\u2010dependent monocytosis during low\u2010dose LCMV infection"],"prefix":"10.1002","volume":"45","author":[{"given":"Matthew B.","family":"Buechler","sequence":"first","affiliation":[{"name":"Department of Immunology University of Washington  Seattle WA USA"},{"name":"Immunology Research Program Benaroya Research Institute (BRI) at Virginia Mason  Seattle WA 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