PMID- 24905956
OWN - NLM
STAT- MEDLINE
DCOM- 20150331
LR  - 20171116
IS  - 1878-5875 (Electronic)
IS  - 1357-2725 (Linking)
VI  - 53
DP  - 2014 Aug
TI  - Dendritic cell subsets involved in type I IFN induction in mouse measles virus 
      infection models.
PG  - 329-33
LID - S1357-2725(14)00144-7 [pii]
LID - 10.1016/j.biocel.2014.05.001 [doi]
AB  - 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.
CI  - Copyright (c) 2014 Elsevier Ltd. All rights reserved.
FAU - Takaki, Hiromi
AU  - Takaki H
AD  - Department of Microbiology and Immunology, Hokkaido University Graduate School of 
      Medicine, Kita-ku, Sapporo 060-8638, Japan. Electronic address: 
      tahiromi@sci.hokudai.ac.jp.
FAU - Oshiumi, Hiroyuki
AU  - Oshiumi H
AD  - Department of Microbiology and Immunology, Hokkaido University Graduate School of 
      Medicine, Kita-ku, Sapporo 060-8638, Japan.
FAU - Matsumoto, Misako
AU  - Matsumoto M
AD  - Department of Microbiology and Immunology, Hokkaido University Graduate School of 
      Medicine, Kita-ku, Sapporo 060-8638, Japan.
FAU - Seya, Tsukasa
AU  - Seya T
AD  - 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.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140604
PL  - Netherlands
TA  - Int J Biochem Cell Biol
JT  - The international journal of biochemistry & cell biology
JID - 9508482
RN  - 0 (Antigens, CD)
RN  - 0 (Interferon Type I)
RN  - 0 (Membrane Cofactor Protein)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (SLAMF1 protein, human)
RN  - 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1)
SB  - IM
MH  - Animals
MH  - Antigens, CD/immunology
MH  - Dendritic Cells/*immunology/virology
MH  - Disease Models, Animal
MH  - Humans
MH  - Immune Tolerance/immunology
MH  - Interferon Type I/genetics/*immunology
MH  - Measles/*genetics/immunology/virology
MH  - Measles virus/*genetics/immunology/pathogenicity
MH  - Membrane Cofactor Protein/immunology
MH  - Mice
MH  - Mice, Transgenic
MH  - Receptors, Cell Surface/immunology
MH  - Signaling Lymphocytic Activation Molecule Family Member 1
OTO - NOTNLM
OT  - Dendritic cells
OT  - Immune suppression
OT  - Measles virus
OT  - Mouse model
OT  - Type I interferon (IFN)
EDAT- 2014/06/07 06:00
MHDA- 2015/04/01 06:00
CRDT- 2014/06/07 06:00
PHST- 2014/03/20 00:00 [received]
PHST- 2014/04/28 00:00 [revised]
PHST- 2014/05/01 00:00 [accepted]
PHST- 2014/06/07 06:00 [entrez]
PHST- 2014/06/07 06:00 [pubmed]
PHST- 2015/04/01 06:00 [medline]
AID - S1357-2725(14)00144-7 [pii]
AID - 10.1016/j.biocel.2014.05.001 [doi]
PST - ppublish
SO  - Int J Biochem Cell Biol. 2014 Aug;53:329-33. doi: 10.1016/j.biocel.2014.05.001. 
      Epub 2014 Jun 4.