PMID- 27142025
OWN - NLM
STAT- MEDLINE
DCOM- 20171213
LR  - 20180110
IS  - 1940-6029 (Electronic)
IS  - 1064-3745 (Linking)
VI  - 1423
DP  - 2016
TI  - Analysis of DC Functions Using CD205-DTR Knock-In Mice.
PG  - 291-308
LID - 10.1007/978-1-4939-3606-9_21 [doi]
AB  - Dendritic cells (DCs) are essential antigen-presenting cells (APCs) that consist 
      of heterogeneous subsets, mainly classified as conventional DCs (cDCs) and 
      plasmacytoid DCs (pDCs). CD205, an endocytic type I C-type lectin-like molecule 
      that belongs to the mannose receptor family, is mainly expressed on CD8alpha(+) cDCs. 
      However, it is unclear how CD205(+) cDCs control immune responses in vivo. To 
      evaluate the contribution of CD205(+) cDCs to the immune system, we engineered 
      knock-in (KI) mice that express the diphtheria toxin receptor (DTR) under the 
      control of the Cd205 gene, which allows the selective conditional ablation of 
      CD205(+) cDCs in vivo. Conditional ablation of CD205(+) cDCs impaired the 
      antigen-specific priming of CD8(+) T cells to generate cytotoxic T lymphocytes 
      (CTLs) mediated through cross presentation of soluble antigen. Upon microbial 
      infection, CD205(+) cDCs contributed to the cross priming of CD8(+) T cells for 
      generating antibacterial CTLs to efficiently eliminate pathogens. Here, we 
      provide a protocol for the generation of bone marrow WT/CD205-DT chimeric mice, 
      depletion of CD205(+) DCs and assessment of depletion efficiency, and protocols 
      for in vivo cross presentation assay, CTL generation assay, and antibacterial 
      immunity assay.
FAU - Fukaya, Tomohiro
AU  - Fukaya T
AD  - Division of Immunology, Department of Infectious Diseases, Faculty of Medicine, 
      University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan.
FAU - Takagi, Hideaki
AU  - Takagi H
AD  - Division of Immunology, Department of Infectious Diseases, Faculty of Medicine, 
      University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan.
FAU - Uto, Tomofumi
AU  - Uto T
AD  - Division of Immunology, Department of Infectious Diseases, Faculty of Medicine, 
      University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan.
FAU - Arimura, Keiichi
AU  - Arimura K
AD  - Division of Immunology, Department of Infectious Diseases, Faculty of Medicine, 
      University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan.
FAU - Sato, Katsuaki
AU  - Sato K
AD  - Division of Immunology, Department of Infectious Diseases, Faculty of Medicine, 
      University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan. 
      katsuaki_sato@med.miyazaki-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Methods Mol Biol
JT  - Methods in molecular biology (Clifton, N.J.)
JID - 9214969
RN  - 0 (Antigens, CD)
RN  - 0 (DEC-205 receptor)
RN  - 0 (Heparin-binding EGF-like Growth Factor)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Minor Histocompatibility Antigens)
RN  - 0 (Receptors, Cell Surface)
SB  - IM
MH  - Animals
MH  - Antigens, CD/*genetics/metabolism
MH  - Bone Marrow Cells/*cytology/immunology
MH  - CD8-Positive T-Lymphocytes/immunology
MH  - Cross-Priming
MH  - Dendritic Cells/*cytology/immunology
MH  - Gene Knock-In Techniques
MH  - Heparin-binding EGF-like Growth Factor/genetics/*metabolism
MH  - Lectins, C-Type/*genetics/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Minor Histocompatibility Antigens/*genetics/metabolism
MH  - Promoter Regions, Genetic
MH  - Receptors, Cell Surface/*genetics/metabolism
MH  - T-Lymphocytes, Cytotoxic/immunology
OTO - NOTNLM
OT  - Cross priming
OT  - Cytotoxic T lymphocytes
OT  - Dendritic cells
OT  - Knock-in mice
OT  - Microbial infection
EDAT- 2016/05/05 06:00
MHDA- 2017/12/14 06:00
CRDT- 2016/05/05 06:00
PHST- 2016/05/05 06:00 [entrez]
PHST- 2016/05/05 06:00 [pubmed]
PHST- 2017/12/14 06:00 [medline]
AID - 10.1007/978-1-4939-3606-9_21 [doi]
PST - ppublish
SO  - Methods Mol Biol. 2016;1423:291-308. doi: 10.1007/978-1-4939-3606-9_21.