PMID- 22736794
OWN - NLM
STAT- MEDLINE
DCOM- 20121005
LR  - 20211021
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Print)
IS  - 0027-8424 (Linking)
VI  - 109
IP  - 28
DP  - 2012 Jul 10
TI  - Conditional ablation of CD205+ conventional dendritic cells impacts the 
      regulation of T-cell immunity and homeostasis in vivo.
PG  - 11288-93
LID - 10.1073/pnas.1202208109 [doi]
AB  - Dendritic cells (DCs) are composed of multiple subsets that play a dual role in 
      inducing immunity and tolerance. However, it is unclear how CD205(+) conventional 
      DCs (cDCs) control immune responses in vivo. Here we generated knock-in mice with 
      the selective conditional ablation of CD205(+) cDCs. CD205(+) cDCs contributed to 
      antigen-specific priming of CD4(+) T cells under steady-state conditions, whereas 
      they were dispensable for antigen-specific CD4(+) T-cell responses under 
      inflammatory conditions. In contrast, CD205(+) cDCs were required for 
      antigen-specific priming of CD8(+) T cells to generate cytotoxic T lymphocytes 
      (CTLs) mediated through cross-presentation. Although CD205(+) cDCs were involved 
      in the thymic generation of CD4(+) regulatory T cells (Tregs), they maintained 
      the homeostasis of CD4(+) Tregs and CD4(+) effector T cells in peripheral and 
      mucosal tissues. On the other hand, CD205(+) cDCs were involved in the 
      inflammation triggered by Toll-like receptor ligand as well as bacterial and 
      viral infections. Upon microbial infections, CD205(+) cDCs contributed to the 
      cross-priming of CD8(+) T cells for generating antimicrobial CTLs to efficiently 
      eliminate pathogens, whereas they suppressed antimicrobial CD4(+) T-cell 
      responses. Thus, these findings reveal a critical role for CD205(+) cDCs in the 
      regulation of T-cell immunity and homeostasis in vivo.
FAU - Fukaya, Tomohiro
AU  - Fukaya T
AD  - Laboratory for Dendritic Cell Immunobiology, RIKEN Research Center for Allergy 
      and Immunology, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
FAU - Murakami, Ryuichi
AU  - Murakami R
FAU - Takagi, Hideaki
AU  - Takagi H
FAU - Sato, Kaori
AU  - Sato K
FAU - Sato, Yumiko
AU  - Sato Y
FAU - Otsuka, Haruna
AU  - Otsuka H
FAU - Ohno, Michiko
AU  - Ohno M
FAU - Hijikata, Atsushi
AU  - Hijikata A
FAU - Ohara, Osamu
AU  - Ohara O
FAU - Hikida, Masaki
AU  - Hikida M
FAU - Malissen, Bernard
AU  - Malissen B
FAU - Sato, Katsuaki
AU  - Sato K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120626
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (3' Untranslated Regions)
RN  - 0 (Antigens, CD)
RN  - 0 (DEC-205 receptor)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Minor Histocompatibility Antigens)
RN  - 0 (Receptors, Cell Surface)
RN  - 147336-22-9 (Green Fluorescent Proteins)
SB  - IM
MH  - 3' Untranslated Regions
MH  - Adaptive Immunity
MH  - Animals
MH  - Antigens, CD/*biosynthesis/chemistry
MH  - CD4-Positive T-Lymphocytes/immunology
MH  - Cross-Priming/immunology
MH  - Dendritic Cells/*cytology
MH  - Green Fluorescent Proteins/metabolism
MH  - Homeostasis
MH  - Humans
MH  - Immune Tolerance/immunology
MH  - Inflammation
MH  - Lectins, C-Type/*biosynthesis/chemistry
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Minor Histocompatibility Antigens
MH  - Receptors, Cell Surface/*biosynthesis/chemistry
MH  - T-Lymphocytes/*immunology
PMC - PMC3396526
COIS- The authors declare no conflict of interest.
EDAT- 2012/06/28 06:00
MHDA- 2012/10/06 06:00
PMCR- 2013/01/10
CRDT- 2012/06/28 06:00
PHST- 2012/06/28 06:00 [entrez]
PHST- 2012/06/28 06:00 [pubmed]
PHST- 2012/10/06 06:00 [medline]
PHST- 2013/01/10 00:00 [pmc-release]
AID - 1202208109 [pii]
AID - 201202208 [pii]
AID - 10.1073/pnas.1202208109 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2012 Jul 10;109(28):11288-93. doi: 
      10.1073/pnas.1202208109. Epub 2012 Jun 26.