Chapter title |
ADP-Ribosylation of P2X7: A Matter of Life and Death for Regulatory T Cells and Natural Killer T Cells.
|
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Chapter number | 420 |
Book title |
Endogenous ADP-Ribosylation
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Published in |
Current topics in microbiology and immunology, July 2014
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DOI | 10.1007/82_2014_420 |
Pubmed ID | |
Book ISBNs |
978-3-31-910770-7, 978-3-31-910771-4
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Authors |
Björn Rissiek, Friedrich Haag, Olivier Boyer, Friedrich Koch-Nolte, Sahil Adriouch, Rissiek, Björn, Haag, Friedrich, Boyer, Olivier, Koch-Nolte, Friedrich, Adriouch, Sahil |
Abstract |
ADP-ribosyltransferases comprise a family of enzymes originally discovered as bacterial toxins and later characterised also in mammals. In mice, the ADP-ribosyltransferase ARTC2.2 is expressed at the surface of T lymphocytes and has been studied extensively. In the presence of extracellular NAD(+), ARTC2.2 ADP-ribosylates several cell surface target proteins and thereby regulates their function. P2X7, an ATP-gated cation channel, has been discovered as a prominent ARTC2.2 target at the surface of mouse T cells. ADP-ribosylation of P2X7 in the presence of low micromolar extracellular NAD(+) induces long-lasting P2X7 activation and triggers cell death. Regulatory T cell subsets (Tregs and NKT cells) are remarkably sensitive to NAD(+)-induced cell death (NICD). Thus, liberation of endogenous NAD(+) by stressed cells is now viewed as a danger signal promoting immune responses by hindering regulatory T cells. This review will highlight the recent discoveries on the in vivo role of the ARTC2.2/P2X7 pathway triggered by the endogenous release of extracellular NAD(+), the relative sensitivity of lymphocytes subsets to this regulatory pathway and its pharmacological manipulation using camelid-derived ARTC2.2-blocking nanobodies. |
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