PMID- 26851221
OWN - NLM
STAT- MEDLINE
DCOM- 20160810
LR  - 20160305
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 196
IP  - 6
DP  - 2016 Mar 15
TI  - Dendritic Cells Regulate GPR34 through Mitogenic Signals and Undergo Apoptosis in 
      Its Absence.
PG  - 2504-13
LID - 10.4049/jimmunol.1501326 [doi]
AB  - Dendritic cells (DCs) are specifically equipped with the G protein-coupled 
      receptor 34 (GPR34). Tight regulation of GPR34 gene expression seems highly 
      important for proper immunological functions, because the absence of this 
      receptor leads to an alteration of the immune response, whereas overexpression 
      was reported to be involved in neuroinflammation. However, the regulatory 
      mechanism of GPR34 expression has not yet been investigated. Whole-transcriptome 
      RNA sequencing analysis from spleens and DCs of GPR34 knockout and wild-type 
      mice, combined with protein-protein interaction data, revealed functional modules 
      affected by the absence of this receptor. Among these, NF-kappaB, MAPK, and 
      apoptosis-signaling pathways showed high significance. Using murine DCs we 
      experimentally show that NF-kappaB and MAPK pathways are involved in the 
      downregulation of GPR34. DCs lacking GPR34 have a higher caspase-3/7 activity and 
      increased apoptosis levels. Our study reveals a novel role of GPR34 in the fate 
      of DCs and identifies a regulatory mechanism that could be relevant for treatment 
      of GPR34-overexpressing pathologies, such as neuroinflammatory or cancer 
      conditions.
CI  - Copyright (c) 2016 by The American Association of Immunologists, Inc.
FAU - Jager, Elisabeth
AU  - Jager E
AD  - Institute of Biochemistry, University of Leipzig, 04103 Leipzig, Germany; 
      Rheumatology Unit, Department of Internal Medicine, University of Leipzig, 04103 
      Leipzig, Germany;
FAU - Schulz, Angela
AU  - Schulz A
AUID- ORCID: 0000-0003-2336-1573
AD  - Institute of Biochemistry, University of Leipzig, 04103 Leipzig, Germany; 
      Integrated Research and Treatment Center Adiposity Diseases, Medical Faculty, 
      University of Leipzig, 04103 Leipzig, Germany; and.
FAU - Lede, Vera
AU  - Lede V
AD  - Institute of Biochemistry, University of Leipzig, 04103 Leipzig, Germany;
FAU - Lin, Chen-Ching
AU  - Lin CC
AD  - Institute of Biomedical Informatics, National Yang-Ming University, Taipei 11221, 
      Taiwan.
FAU - Schoneberg, Torsten
AU  - Schoneberg T
AD  - Institute of Biochemistry, University of Leipzig, 04103 Leipzig, Germany; 
      schoberg@medizin.uni-leipzig.de diana_leduc@eva.mpg.de.
FAU - Le Duc, Diana
AU  - Le Duc D
AUID- ORCID: 0000-0001-7289-2552
AD  - Institute of Biochemistry, University of Leipzig, 04103 Leipzig, Germany; 
      schoberg@medizin.uni-leipzig.de diana_leduc@eva.mpg.de.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160205
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (G-protein-coupled receptor 34)
RN  - 0 (Receptors, Lysophospholipid)
SB  - IM
MH  - Animals
MH  - Apoptosis/*immunology
MH  - Blotting, Western
MH  - Dendritic Cells/*immunology
MH  - Flow Cytometry
MH  - Gene Expression Regulation/immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Receptors, Lysophospholipid/*immunology
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2016/02/07 06:00
MHDA- 2016/08/11 06:00
CRDT- 2016/02/07 06:00
PHST- 2015/06/12 00:00 [received]
PHST- 2016/01/03 00:00 [accepted]
PHST- 2016/02/07 06:00 [entrez]
PHST- 2016/02/07 06:00 [pubmed]
PHST- 2016/08/11 06:00 [medline]
AID - jimmunol.1501326 [pii]
AID - 10.4049/jimmunol.1501326 [doi]
PST - ppublish
SO  - J Immunol. 2016 Mar 15;196(6):2504-13. doi: 10.4049/jimmunol.1501326. Epub 2016 
      Feb 5.