TY - JOUR
T1 - Virus-triggered ATP release limits viral replication through facilitating IFN-β production in a P2X7-dependent manner
AU - Zhang, Chengfei
AU - He, Hongwang
AU - Wang, Li
AU - Zhang, Na
AU - Huang, Hongjun
AU - Xiong, Qingqing
AU - Yan, Yan
AU - Wu, Nannan
AU - Ren, Hua
AU - Han, Honghui
AU - Liu, Mingyao
AU - Qian, Min
AU - Du, Bing
N1 - Publisher Copyright:
Copyright © 2017 by The American Association of Immunologists, Inc.
PY - 2017/8/15
Y1 - 2017/8/15
N2 - Accumulating evidence shows that innate immune responses are associated with extracellular nucleotides, particularly ATP. In this article, we demonstrate extensive protection of ATP/P2X7 signaling in a host against viral infection. Interestingly, we observed a significant increase in ATP as a danger signal in vesicular stomatitis virus (VSV)-infected cell supernatant and VSV-infected mice in an exocytosis-and pannexin channel-dependent manner. Furthermore, extracellular ATP reduces the replication of VSV, Newcastle disease virus, murine leukemia virus, and HSV in vivo and in vitro through the P2X7 receptor. Meanwhile, ATP significantly increases IFN-β expression in a concentration-and time-dependent manner. Mechanistically, ATP facilitates IFN-β secretion through P38/JNK/ATF-2 signaling pathways, which are crucial in promoting antiviral immunity. Taken together, these results demonstrate the protective role of extracellular ATP and P2X7 in viral infection and suggest a potential therapeutic role for ATP/P2X7 in viral diseases.
AB - Accumulating evidence shows that innate immune responses are associated with extracellular nucleotides, particularly ATP. In this article, we demonstrate extensive protection of ATP/P2X7 signaling in a host against viral infection. Interestingly, we observed a significant increase in ATP as a danger signal in vesicular stomatitis virus (VSV)-infected cell supernatant and VSV-infected mice in an exocytosis-and pannexin channel-dependent manner. Furthermore, extracellular ATP reduces the replication of VSV, Newcastle disease virus, murine leukemia virus, and HSV in vivo and in vitro through the P2X7 receptor. Meanwhile, ATP significantly increases IFN-β expression in a concentration-and time-dependent manner. Mechanistically, ATP facilitates IFN-β secretion through P38/JNK/ATF-2 signaling pathways, which are crucial in promoting antiviral immunity. Taken together, these results demonstrate the protective role of extracellular ATP and P2X7 in viral infection and suggest a potential therapeutic role for ATP/P2X7 in viral diseases.
UR - https://www.scopus.com/pages/publications/85027362466
U2 - 10.4049/jimmunol.1700187
DO - 10.4049/jimmunol.1700187
M3 - 文章
C2 - 28687662
AN - SCOPUS:85027362466
SN - 0022-1767
VL - 199
SP - 1372
EP - 1381
JO - Journal of Immunology
JF - Journal of Immunology
IS - 4
ER -