PMID- 22236403
OWN - NLM
STAT- MEDLINE
DCOM- 20120627
LR  - 20211021
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Print)
IS  - 0019-2805 (Linking)
VI  - 136
IP  - 2
DP  - 2012 Jun
TI  - Bile acids induce monocyte differentiation toward interleukin-12 hypo-producing 
      dendritic cells via a TGR5-dependent pathway.
PG  - 153-62
LID - 10.1111/j.1365-2567.2012.03554.x [doi]
AB  - Dendritic cells (DCs) are known as antigen-presenting cells and play a central 
      role in both innate and acquired immunity. Peripheral blood monocytes give rise 
      to resident and recruited DCs in lymph nodes and non-lymphoid tissues. The 
      ligands of nuclear hormone receptors can modulate DC differentiation and so 
      influence various biological functions of DCs. The role of bile acids (BAs) as 
      signalling molecules has recently become apparent, but the functional role of BAs 
      in DC differentiation has not yet been elucidated. We show that DCs derived from 
      human peripheral blood monocytes cultured with a BA produce lower levels of 
      interleukin-12 (IL-12) and tumour necrosis factor-alpha in response to stimulation 
      with commensal bacterial antigens. Stimulation through the nuclear receptor 
      farnesoid X (FXR) did not affect the differentiation of DCs. However, DCs 
      differentiated with the specific agonist for TGR5, a transmembrane BA receptor, 
      showed an IL-12 hypo-producing phenotype. Expression of TGR5 could only be 
      identified in monocytes and was rapidly down-regulated during monocyte 
      differentiation to DCs. Stimulation with 8-bromoadenosine-cyclic AMP (8-Br-cAMP), 
      which acts downstream of TGR5 signalling, also promoted differentiation into 
      IL-12 hypo-producing DCs. These results indicate that BAs induce the 
      differentiation of IL-12 hypo-producing DCs from monocytes via the TGR5-cAMP 
      pathway.
CI  - (c) 2012 The Authors. Immunology (c) 2012 Blackwell Publishing Ltd.
FAU - Ichikawa, Riko
AU  - Ichikawa R
AD  - Division of Gastroenterology and Hepatology, Department of Internal Medicine, 
      School of Medicine, Keio University, Tokyo, Japan.
FAU - Takayama, Tetsuro
AU  - Takayama T
FAU - Yoneno, Kazuaki
AU  - Yoneno K
FAU - Kamada, Nobuhiko
AU  - Kamada N
FAU - Kitazume, Mina T
AU  - Kitazume MT
FAU - Higuchi, Hajime
AU  - Higuchi H
FAU - Matsuoka, Katsuyoshi
AU  - Matsuoka K
FAU - Watanabe, Mitsuhiro
AU  - Watanabe M
FAU - Itoh, Hiroshi
AU  - Itoh H
FAU - Kanai, Takanori
AU  - Kanai T
FAU - Hisamatsu, Tadakazu
AU  - Hisamatsu T
FAU - Hibi, Toshifumi
AU  - Hibi T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Bile Acids and Salts)
RN  - 0 (GPBAR1 protein, human)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 187348-17-0 (Interleukin-12)
RN  - 23583-48-4 (8-Bromo Cyclic Adenosine Monophosphate)
SB  - IM
MH  - 8-Bromo Cyclic Adenosine Monophosphate/pharmacology
MH  - Bile Acids and Salts/*immunology/metabolism
MH  - Cell Differentiation/drug effects/immunology
MH  - Cells, Cultured
MH  - Dendritic Cells/*immunology/metabolism
MH  - Down-Regulation
MH  - Humans
MH  - Interleukin-12/biosynthesis/*immunology
MH  - Leukocytes, Mononuclear/*immunology/metabolism
MH  - Receptors, G-Protein-Coupled/agonists/*immunology
MH  - Tumor Necrosis Factor-alpha/biosynthesis/immunology
PMC - PMC3403261
EDAT- 2012/01/13 06:00
MHDA- 2012/06/28 06:00
PMCR- 2013/06/01
CRDT- 2012/01/13 06:00
PHST- 2012/01/13 06:00 [entrez]
PHST- 2012/01/13 06:00 [pubmed]
PHST- 2012/06/28 06:00 [medline]
PHST- 2013/06/01 00:00 [pmc-release]
AID - 10.1111/j.1365-2567.2012.03554.x [doi]
PST - ppublish
SO  - Immunology. 2012 Jun;136(2):153-62. doi: 10.1111/j.1365-2567.2012.03554.x.