title: Dendritic cell subsets involved in type I IFN induction in mouse measles virus infection models.
abstract: Measles caused by measles virus (MV) infection remains important in child mortality. Although the natural host of MV is human, mouse models expressing MV entry receptors (human CD46, CD150) and disrupting the interferon (IFN) pathways work for investigating immune responses during early MV infection in vivo. Dendritic cells (DCs) are primary targets for MV in the mouse models and are efficiently infected with several MV strains in the respiratory tract in vivo. However, questions remain about what kind of DC in a variety of DC subsets is involved in initial MV infection and how the RNA sensors evoke circumventing signals against MV in infected DCs. Since type I IFN-inducing pathways are a pivotal defense system that leads to the restriction of systemic viral infection, we have generated CD150-transgenic mice with disrupting each of the IFN-inducing pathway, and clarified that DC subsets had subset-specific IFN-inducing systems, which critically determined the DC's differential susceptibility to MV.
authors.affiliation: Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo 060-8638, Japan. Electronic address: tahiromi@sci.hokudai.ac.jp.
authors.forename: Hiromi
authors.initials: H
authors.lastname: Takaki
authors.affiliation: Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo 060-8638, Japan.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Oshiumi
authors.affiliation: Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo 060-8638, Japan.
authors.forename: Misako
authors.initials: M
authors.lastname: Matsumoto
authors.affiliation: Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo 060-8638, Japan. Electronic address: seya-tu@pop.med.hokudai.ac.jp.
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Seya
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology* / Q000821:virology; D004195:Disease Models, Animal; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D007370:Interferon Type I / Q000235:genetics / Q000276:immunology*; D008457:Measles / Q000235:genetics* / Q000276:immunology / Q000821:virology; D008459:Measles virus / Q000235:genetics* / Q000276:immunology / Q000472:pathogenicity; D051916:Membrane Cofactor Protein / Q000276:immunology; D051379:Mice; D008822:Mice, Transgenic; D011956:Receptors, Cell Surface / Q000276:immunology; D000071177:Signaling Lymphocytic Activation Molecule Family Member 1
chemical_list: D015703:Antigens, CD; D007370:Interferon Type I; D051916:Membrane Cofactor Protein; D011956:Receptors, Cell Surface; C000604059:SLAMF1 protein, human; D000071177:Signaling Lymphocytic Activation Molecule Family Member 1
keywords: Dendritic cells; Immune suppression; Measles virus; Mouse model; Type I interferon (IFN)