PMID- 23670193
OWN - NLM
STAT- MEDLINE
DCOM- 20130812
LR  - 20221109
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 190
IP  - 12
DP  - 2013 Jun 15
TI  - Critical roles of a dendritic cell subset expressing a chemokine receptor, XCR1.
PG  - 6071-82
LID - 10.4049/jimmunol.1202798 [doi]
AB  - Dendritic cells (DCs) consist of various subsets that play crucial roles in 
      linking innate and adaptive immunity. In the murine spleen, CD8alpha(+) DCs exhibit a 
      propensity to ingest dying/dead cells, produce proinflammatory cytokines, and 
      cross-present Ags to generate CD8(+) T cell responses. To track and ablate 
      CD8alpha(+) DCs in vivo, we generated XCR1-venus and XCR1-DTRvenus mice, in which 
      genes for a fluorescent protein, venus, and a fusion protein consisting of 
      diphtheria toxin receptor and venus were knocked into the gene locus of a 
      chemokine receptor, XCR1, which is highly expressed in CD8alpha(+) DCs. In both mice, 
      venus(+) cells were detected in the majority of CD8alpha(+) DCs, but they were not 
      detected in any other cells, including splenic macrophages. Venus(+)CD8alpha(+) DCs 
      were superior to venus(-)CD8alpha(+) DCs with regard to their cytokine-producing 
      ability in response to TLR stimuli. In other tissues, venus(+) cells were found 
      primarily in lymph node (LN)-resident CD8alpha(+), LN migratory and peripheral 
      CD103(+) DCs, which are closely related to splenic CD8alpha(+) DCs, although some 
      thymic CD8alpha(-)CD11b(-) and LN CD103(-)CD11b(-) DCs were also venus(+). In 
      response to dsRNAs, diphtheria toxin-treated XCR1-DTR mice showed impaired CD8(+) 
      T cell responses, with retained cytokine and augmented CD4(+) T cell responses. 
      Furthermore, Listeria monocytogenes infection and anti-L. monocytogenes CD8(+) T 
      cell responses were defective in diphtheria toxin-treated XCR1-DTRvenus mice. 
      Thus, XCR1-expressing DCs were required for dsRNA- or bacteria-induced CD8(+) T 
      cell responses. XCR1-venus and XCR1-DTRvenus mice should be useful for 
      elucidating the functions and behavior of XCR1-expressing DCs, including CD8alpha(+) 
      and CD103(+) DCs, in lymphoid and peripheral tissues.
FAU - Yamazaki, Chihiro
AU  - Yamazaki C
AD  - Laboratory for Host Defense, RIKEN Research Center for Allergy and Immunology, 
      Yokohama, Kanagawa 230-0045, Japan.
FAU - Sugiyama, Masanaka
AU  - Sugiyama M
FAU - Ohta, Tomokazu
AU  - Ohta T
FAU - Hemmi, Hiroaki
AU  - Hemmi H
FAU - Hamada, Eri
AU  - Hamada E
FAU - Sasaki, Izumi
AU  - Sasaki I
FAU - Fukuda, Yuri
AU  - Fukuda Y
FAU - Yano, Takahiro
AU  - Yano T
FAU - Nobuoka, Mikako
AU  - Nobuoka M
FAU - Hirashima, Takeshi
AU  - Hirashima T
FAU - Iizuka, Akihiko
AU  - Iizuka A
FAU - Sato, Katsuaki
AU  - Sato K
FAU - Tanaka, Takashi
AU  - Tanaka T
FAU - Hoshino, Katsuaki
AU  - Hoshino K
FAU - Kaisho, Tsuneyasu
AU  - Kaisho T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130513
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Bacterial Proteins)
RN  - 0 (Luminescent Proteins)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (XC chemokine receptor 1, mouse)
RN  - 0 (yellow fluorescent protein, Bacteria)
SB  - IM
MH  - Animals
MH  - Antigen Presentation/immunology
MH  - Bacterial Proteins/genetics/metabolism
MH  - Cell Separation
MH  - Cross-Priming/*immunology
MH  - Dendritic Cells/*immunology/metabolism
MH  - Flow Cytometry
MH  - Gene Knock-In Techniques
MH  - Luminescent Proteins/genetics/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Receptors, Chemokine/*immunology/metabolism
EDAT- 2013/05/15 06:00
MHDA- 2013/08/13 06:00
CRDT- 2013/05/15 06:00
PHST- 2013/05/15 06:00 [entrez]
PHST- 2013/05/15 06:00 [pubmed]
PHST- 2013/08/13 06:00 [medline]
AID - jimmunol.1202798 [pii]
AID - 10.4049/jimmunol.1202798 [doi]
PST - ppublish
SO  - J Immunol. 2013 Jun 15;190(12):6071-82. doi: 10.4049/jimmunol.1202798. Epub 2013 
      May 13.