Source:http://linkedlifedata.com/resource/pubmed/id/17579037
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2007-6-20
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| pubmed:abstractText |
Mono ADP-ribosyltransferase 2 (ART2) is an ectoenzyme expressed on mouse T lymphocytes, which catalyze the transfer of ADP-ribose groups from NAD(+) onto several target proteins. In vitro, ADP-ribosylation by ART2 activates the P2X7 ATP receptor and is responsible for NAD(+)-induced T cell death (NICD). Yet, the origin of extracellular NAD(+) and the role of NICD in vivo remain elusive. In a model of acute inflammation induced by polyacrylamide beads, we demonstrate release of NAD(+) into exudates during the early phase of the inflammatory response. This leads to T cell depletion in the draining lymph nodes from wild-type and, more severely, from mice lacking the CD38 NAD(+) glycohydrolase, whereas no effect is observed in ART2-deficient animals. Intravenous injection of NAD(+) used to exacerbate NICD in vivo results in fast and dramatic ART2- and P2X7-dependent depletion of CD4+ and CD8+ T lymphocytes, which can affect up to 80% of peripheral T cells in CD38(-/-) mice. This affects mainly naive T cells as most cells surviving in vivo NAD+ treatment exhibit the phenotype of recently activated/memory cells. Consistently, treatment with NAD(+) abolishes primary Ab response to a T-dependent Ag in NICD-susceptible CD38(-/-) mice but has no effect on the secondary response when given several days after priming. Unexpectedly NAD+ treatment improves the response in their wild-type BALB/c counterparts. We propose that NAD(+) released during early inflammation facilitates the expansion of primed T cells, through ART2-driven death of resting cells, thus contributing to the dynamic regulation of T cell homeostasis.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/ADP Ribose Transferases,
http://linkedlifedata.com/resource/pubmed/chemical/Art2a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Art2b protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/NAD
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
179
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
186-94
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| pubmed:dateRevised |
2009-9-4
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| pubmed:meshHeading |
pubmed-meshheading:17579037-ADP Ribose Transferases,
pubmed-meshheading:17579037-Acute Disease,
pubmed-meshheading:17579037-Animals,
pubmed-meshheading:17579037-Apoptosis,
pubmed-meshheading:17579037-Cell Death,
pubmed-meshheading:17579037-G0 Phase,
pubmed-meshheading:17579037-Homeostasis,
pubmed-meshheading:17579037-Immunologic Memory,
pubmed-meshheading:17579037-Immunophenotyping,
pubmed-meshheading:17579037-Inflammation Mediators,
pubmed-meshheading:17579037-Injections, Intravenous,
pubmed-meshheading:17579037-Lymphocyte Activation,
pubmed-meshheading:17579037-Lymphocyte Depletion,
pubmed-meshheading:17579037-Mice,
pubmed-meshheading:17579037-Mice, Inbred BALB C,
pubmed-meshheading:17579037-Mice, Knockout,
pubmed-meshheading:17579037-NAD,
pubmed-meshheading:17579037-Oxidation-Reduction,
pubmed-meshheading:17579037-T-Lymphocyte Subsets
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| pubmed:year |
2007
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| pubmed:articleTitle |
NAD+ released during inflammation participates in T cell homeostasis by inducing ART2-mediated death of naive T cells in vivo.
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| pubmed:affiliation |
University Denis Diderot-Paris 7, EA 1556 Paris, France.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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