PMID- 22379034
OWN - NLM
STAT- MEDLINE
DCOM- 20120604
LR  - 20181201
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 188
IP  - 7
DP  - 2012 Apr 1
TI  - Stimulation of dopamine receptor D5 expressed on dendritic cells potentiates 
      Th17-mediated immunity.
PG  - 3062-70
LID - 10.4049/jimmunol.1103096 [doi]
AB  - Dendritic cells (DCs) are responsible for priming T cells and for promoting their 
      differentiation from naive T cells into appropriate effector cells. Emerging 
      evidence suggests that neurotransmitters can modulate T cell-mediated immunity. 
      However, the involvement of specific neurotransmitters or receptors remains 
      poorly understood. In this study, we analyzed the role of dopamine in the 
      regulation of DC function. We found that DCs express dopamine receptors as well 
      as the machinery necessary to synthesize, store, and degrade dopamine. Notably, 
      the expression of D5R decreased upon LPS-induced DC maturation. Deficiency of D5R 
      on the surface of DCs impaired LPS-induced IL-23 and IL-12 production and 
      consequently attenuated the activation and proliferation of Ag-specific CD4(+) T 
      cells. To determine the relevance of D5R expressed on DCs in vivo, we studied the 
      role of this receptor in the modulation of a CD4(+) T cell-driven autoimmunity 
      model. Importantly, D5R-deficient DCs prophylactically transferred into wild-type 
      recipients were able to reduce the severity of experimental autoimmune 
      encephalomyelitis. Furthermore, mice transferred with D5R-deficient DCs displayed 
      a significant reduction in the percentage of Th17 cells infiltrating the CNS 
      without differences in the percentage of Th1 cells compared with animals 
      transferred with wild-type DCs. Our findings demonstrate that by contributing to 
      CD4(+) T cell activation and differentiation to Th17 phenotype, D5R expressed on 
      DCs is able to modulate the development of an autoimmune response in vivo.
FAU - Prado, Carolina
AU  - Prado C
AD  - Fundacion Ciencia y Vida, Santiago, Chile.
FAU - Contreras, Francisco
AU  - Contreras F
FAU - Gonzalez, Hugo
AU  - Gonzalez H
FAU - Diaz, Pablo
AU  - Diaz P
FAU - Elgueta, Daniela
AU  - Elgueta D
FAU - Barrientos, Magaly
AU  - Barrientos M
FAU - Herrada, Andres A
AU  - Herrada AA
FAU - Lladser, Alvaro
AU  - Lladser A
FAU - Bernales, Sebastian
AU  - Bernales S
FAU - Pacheco, Rodrigo
AU  - Pacheco R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120229
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Cytokines)
RN  - 0 (Drd5 protein, mouse)
RN  - 0 (Interleukin-17)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 137750-35-7 (Receptors, Dopamine D5)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Autocrine Communication/immunology
MH  - CD4-Positive T-Lymphocytes/immunology
MH  - Cell Differentiation
MH  - Coculture Techniques
MH  - Cytokines/biosynthesis/genetics
MH  - Dendritic Cells/drug effects/*immunology/metabolism/transplantation
MH  - Dopamine/metabolism/pharmacology/*physiology
MH  - Encephalomyelitis, Autoimmune, Experimental/*immunology/therapy
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Immunity, Cellular
MH  - Interleukin-17/biosynthesis/genetics
MH  - Lipopolysaccharides/pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Receptors, Dopamine D5/agonists/biosynthesis/genetics/*physiology
MH  - Specific Pathogen-Free Organisms
MH  - Th17 Cells/*immunology
EDAT- 2012/03/02 06:00
MHDA- 2012/06/05 06:00
CRDT- 2012/03/02 06:00
PHST- 2012/03/02 06:00 [entrez]
PHST- 2012/03/02 06:00 [pubmed]
PHST- 2012/06/05 06:00 [medline]
AID - jimmunol.1103096 [pii]
AID - 10.4049/jimmunol.1103096 [doi]
PST - ppublish
SO  - J Immunol. 2012 Apr 1;188(7):3062-70. doi: 10.4049/jimmunol.1103096. Epub 2012 
      Feb 29.