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Triggering of T‐Cell Apoptosis by Toxin‐Related Ecto‐ADP‐Ribosyltransferase ART2
Author(s) -
SCHEUPLEIN FELIX,
ADRIOUCH SAHAHIL,
GlOWACKI GUSTAVO,
HAAG FRIEDRICH,
SEMAN MICHEL,
KOCHNOLTE FRIEDRICH
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1299.051
Subject(s) - nad+ kinase , phosphatidylserine , adp ribosylation , cytolysis , intracellular , apoptosis , microbiology and biotechnology , dna fragmentation , programmed cell death , biology , extracellular , propidium iodide , chemistry , biochemistry , cytotoxicity , enzyme , membrane , in vitro , phospholipid
A bstract : Cytotoxicity induced by protein ADP‐ribosylation is a common theme of certain bacterial toxins and of the mammalian ectoenzyme ART2. Exposure of T cells to NAD, the substrate for ART2‐catalyzed ADP‐ribosylation, induces exposure of phosphatidylserine, uptake of propidium iodide, and fragmentation of DNA. ART2‐specific antibodies raised by gene gun immunization block NAD‐induced apoptosis. ART2 catalyzed ADP‐ribosylation of cell membrane proteins induces formation of cytolytic membrane pores by activating the P2X7 purinoceptor. This alternative pathway to T cell apoptosis could be triggered upon the release of NAD from intracellular stores, for example, during inflammatory tissue damage.