PMID- 32554432
OWN - NLM
STAT- MEDLINE
DCOM- 20210315
LR  - 20210315
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 205
IP  - 2
DP  - 2020 Jul 15
TI  - P2Y(6) Deficiency Enhances Dendritic Cell-Mediated Th1/Th17 Differentiation and 
      Aggravates Experimental Autoimmune Encephalomyelitis.
PG  - 387-397
LID - 10.4049/jimmunol.1900916 [doi]
AB  - Dendritic cells (DCs) are essential APCs and play a crucial role in initiating 
      and regulating the adaptive immune response. In this study, we have reported that 
      P2Y(6), a member of G protein-coupled receptors, inhibits the maturation and 
      activation of DCs via suppressing the activation of the transcription factor 
      NF-kappaB. Furthermore, loss of P2Y(6) does not impact T cells homeostasis in the 
      steady-state. However, in vitro studies show that P2Y(6) signaling inhibits the 
      production of IL-12 and IL-23 and the polarization of Th1 and Th17 subsets 
      mediated by DCs. In addition, we find that mice lacking P2Y(6) develop more 
      severe experimental autoimmune encephalomyelitis compared with wild-type mice. 
      Our results indicate that P2Y(6) functions as a pivotal regulator on DC 
      maturation, and the loss of P2Y(6) results in the aggravated experimental 
      autoimmune encephalomyelitis, which suggests that P2Y(6) may play a pivotal role 
      in the pathogenesis of autoimmune diseases.
CI  - Copyright (c) 2020 by The American Association of Immunologists, Inc.
FAU - Li, Zhenlong
AU  - Li Z
AD  - Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East 
      China Normal University, Shanghai 200241, China.
FAU - He, Cong
AU  - He C
AD  - Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East 
      China Normal University, Shanghai 200241, China.
FAU - Zhang, Jiang
AU  - Zhang J
AUID- ORCID: 0000-0001-7392-8270
AD  - Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East 
      China Normal University, Shanghai 200241, China.
FAU - Zhang, Hongmei
AU  - Zhang H
AD  - Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East 
      China Normal University, Shanghai 200241, China.
FAU - Wei, Huan
AU  - Wei H
AUID- ORCID: 0000-0003-3916-5518
AD  - Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East 
      China Normal University, Shanghai 200241, China.
FAU - Wu, Shijia
AU  - Wu S
AD  - Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East 
      China Normal University, Shanghai 200241, China.
FAU - Jiang, Wenzheng
AU  - Jiang W
AUID- ORCID: 0000-0003-4999-4168
AD  - Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East 
      China Normal University, Shanghai 200241, China wzjiang@bio.ecnu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200617
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Interleukin-23)
RN  - 0 (Receptors, Purinergic P2)
RN  - 0 (purinoceptor P2Y6)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Animals
MH  - Cell Differentiation
MH  - Cells, Cultured
MH  - Dendritic Cells/*immunology
MH  - Disease Models, Animal
MH  - Encephalomyelitis, Autoimmune, Experimental/*immunology
MH  - Humans
MH  - Interleukin-12/metabolism
MH  - Interleukin-23/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Multiple Sclerosis/*immunology
MH  - Receptors, Purinergic P2/genetics/*metabolism
MH  - Signal Transduction
MH  - Th1 Cells/*immunology
MH  - Th17 Cells/*immunology
EDAT- 2020/06/20 06:00
MHDA- 2021/03/16 06:00
CRDT- 2020/06/20 06:00
PHST- 2019/08/01 00:00 [received]
PHST- 2020/05/14 00:00 [accepted]
PHST- 2020/06/20 06:00 [pubmed]
PHST- 2021/03/16 06:00 [medline]
PHST- 2020/06/20 06:00 [entrez]
AID - jimmunol.1900916 [pii]
AID - 10.4049/jimmunol.1900916 [doi]
PST - ppublish
SO  - J Immunol. 2020 Jul 15;205(2):387-397. doi: 10.4049/jimmunol.1900916. Epub 2020 
      Jun 17.