PMID- 25458315
OWN - NLM
STAT- MEDLINE
DCOM- 20150305
LR  - 20181202
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 63
IP  - 2
DP  - 2015 Feb
TI  - Adenosine A2A receptor, a potential valuable target for controlling reoxygenated 
      DCs-triggered inflammation.
PG  - 559-65
AB  - Dendritic cells (DCs) exposed to various oxygen tensions under physiopathological 
      conditions are the critical immune cells linking innate and adaptive immunity. We 
      have previously demonstrated that reoxygenation of hypoxia-differentiated DCs 
      triggers complete DCs activation and inflammatory responses, so restraining the 
      activation of reoxygenated DCs is important to suppress inflammatory responses in 
      diseases caused by oxygen redelivery such as ischemia-reperfusion injury. In the 
      current study, we showed that reoxygenation of hypoxia-differentiated DCs led to 
      predominant expression of high levels of adenosine receptor A2AR on reoxygenated 
      DCs as compared to those on hypoxic or normoxic DCs. Agonist CGS21680 targeting 
      A2AR could effectively inhibit the maturation and activation of reoxygenated DCs 
      through downregulating the expression of MHC class II molecules and CD86. In 
      response to CGS21680 treatment, reoxygenated DCs exhibited a decrease in 
      proinflammatory cytokines IL-1beta, IL-6 and TNF-alpha, and an increase in 
      immune-regulatory cytokine TGF-beta. These data suggest the critical role of A2AR 
      signaling pathway in inhibiting the maturation and proinflammatory function of 
      reoxygenated DCs, thereby proposing A2AR as a potential valuable target for 
      controlling reoxygenated DCs-triggered inflammation.
FAU - Liu, Chunmei
AU  - Liu C
AD  - Department of Immunology, Shandong University School of Medicine, Jinan 250012, 
      Shandong, PR China
FAU - Shang, Qianwen
AU  - Shang Q
FAU - Bai, Yang
AU  - Bai Y
FAU - Guo, Chun
AU  - Guo C
FAU - Zhu, Faliang
AU  - Zhu F
FAU - Zhang, Lining
AU  - Zhang L
FAU - Wang, Qun
AU  - Wang Q
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Phenethylamines)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Adenosine A2A)
RN  - 120225-54-9 (2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine)
RN  - K72T3FS567 (Adenosine)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Adenosine/analogs & derivatives/pharmacology
MH  - Animals
MH  - Cell Differentiation/drug effects/genetics
MH  - Cytokines/metabolism
MH  - Dendritic Cells/drug effects/*metabolism
MH  - Female
MH  - Inflammation/genetics/*metabolism/*pathology
MH  - Inflammation Mediators/metabolism
MH  - Mice, Inbred C57BL
MH  - Models, Biological
MH  - *Molecular Targeted Therapy
MH  - Oxygen/*pharmacology
MH  - Phenethylamines/pharmacology
MH  - Phenotype
MH  - RNA, Messenger/genetics/metabolism
MH  - Receptor, Adenosine A2A/genetics/*metabolism
MH  - Signal Transduction/drug effects/genetics
MH  - Up-Regulation/drug effects
EDAT- 2014/12/03 06:00
MHDA- 2015/03/07 06:00
CRDT- 2014/12/03 06:00
PHST- 2014/05/26 00:00 [received]
PHST- 2014/09/22 00:00 [revised]
PHST- 2014/10/12 00:00 [accepted]
PHST- 2014/12/03 06:00 [entrez]
PHST- 2014/12/03 06:00 [pubmed]
PHST- 2015/03/07 06:00 [medline]
AID - S0161-5890(14)00277-6 [pii]
AID - 10.1016/j.molimm.2014.10.012 [doi]
PST - ppublish
SO  - Mol Immunol. 2015 Feb;63(2):559-65. doi: 10.1016/j.molimm.2014.10.012.