The role of pannexin1 in the induction and resolution of inflammation.
The role of pannexin1 in the induction and resolution of inflammation.
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DOI:
10.1016/j.febslet.2014.03.009
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发表时间:
2014-04-17
期刊:
影响因子:
3.5
通讯作者:
Leitinger N
中科院分区:
文献类型:
--
作者:
Adamson SE;Leitinger N
Extracellular ATP is an important signaling molecule throughout the inflammatory cascade, serving as a danger signal that causes activation of the inflammasome, enhancement of immune cell infiltration, and fine-tuning of several signaling cascades including those important for the resolution of inflammation. Recent studies demonstrated that ATP can be released from cells in a controlled manner through pannexin (Panx) channels. Panx1-mediated ATP release is involved in inflammasome activation and neutrophil/macrophage chemotaxis, activation of T cells, and a role for Panx1 in inducing and propagating inflammation has been demonstrated in various organs, including lung and the central and peripheral nervous system. The recognition and clearance of dying cells and debris from focal points of inflammation is critical in the resolution of inflammation, and Panx1-mediated ATP release from dying cells has been shown to recruit phagocytes. Moreover, extracellular ATP can be broken down by ectonucleotidases into ADP, AMP, and adenosine, which is critical in the resolution of inflammation. Together, Panx1, ATP, purinergic receptors, and ectonucleotidases contribute to important feedback loops during the inflammatory response, and thus represent promising candidates for new therapies.
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影响因子:
3.3
作者:
Barat, Corinne;Gilbert, Caroline;Imbeault, Michael;Tremblay, Michel J.
通讯作者:
Tremblay, Michel J.
影响因子:
20.3
作者:
Borsellino, Giovanna;Kleinewietfeld, Markus;Falk, Kirsten
通讯作者:
Falk, Kirsten
影响因子:
64.8
作者:
通讯作者:
--
DOI:
10.4049/jimmunol.1000108
发表时间:
2010-08-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Ernst PB;Garrison JC;Thompson LF
通讯作者:
Thompson LF
影响因子:
20.1
作者:
Billaud M;Lohman AW;Straub AC;Looft-Wilson R;Johnstone SR;Araj CA;Best AK;Chekeni FB;Ravichandran KS;Penuela S;Laird DW;Isakson BE
通讯作者:
Isakson BE