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Titolo:
Rapid induction of naive T cell apoptosis by ecto-nicotinamide adenine dinucleotide: Requirement for mono(ADP-ribosyl)Transferase 2 and a downstream effector
Autore:
Adriouch, S; Ohlrogge, W; Haag, F; Koch-Nolte, F; Seman, M;
Indirizzi:
Univ Paris 07, Lab Immunodifferenciat, EA 1556, F-75251 Paris 05, France Univ Paris 07 Paris France 05 renciat, EA 1556, F-75251 Paris 05, France Univ Hamburg Hosp, Inst Immunol, D-2000 Hamburg, Germany Univ Hamburg Hosp Hamburg Germany D-2000 mmunol, D-2000 Hamburg, Germany
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 1, volume: 167, anno: 2001,
pagine: 196 - 203
SICI:
0022-1767(20010701)167:1<196:RIONTC>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
RIBOSYLATING BACTERIAL TOXINS; ADP-RIBOSYLTRANSFERASE; MOLECULAR CHARACTERIZATION; MARKER RT6; SIGNAL-TRANSDUCTION; GENE FAMILY; EXPRESSION; ACTIVATION; MOUSE; LYMPHOCYTES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Seman, M Univ Paris 07, Lab Immunodifferenciat, EA 1556, CP 7124,Tour 54,2Pl Jussieu, F-75251 Paris 05, France Univ Paris 07 CP 7124,Tour 54,2 Pl Jussieu Paris France 05 rance
Citazione:
S. Adriouch et al., "Rapid induction of naive T cell apoptosis by ecto-nicotinamide adenine dinucleotide: Requirement for mono(ADP-ribosyl)Transferase 2 and a downstream effector", J IMMUNOL, 167(1), 2001, pp. 196-203

Abstract

Lymphocytes express a number of NAD-metabolizing ectoenzymes, including mono(ADP-ribosyl)transferases (ART) and ADP ribosylcyclases. These enzymes may regulate lymphocyte functions following the release of NAD in injured or inflammatory tissues We report here that extracellular NAD induces apoptosis in BALB/c splenic T cells with an IC50 of 3-5 muM. Annexin V staining of cells was observed already 10 min after treatment with NAD in the absence of any additional signal. Removal of GPI-anchored cell surface proteins by phosphatidylinositol-specific phospholipase C treatment rendered cells resistant to NAD-mediated apoptosis. RT-PCR analyses revealed that resting BALB/c T cells expressed the genes for GPI-anchored ART2.1 and ART2.2 but not ART1. ART2-specific antisera blocked radiolabeling of cell surface proteins with both [P-32]NAD and NAD-mediated apoptosis. Further analyses revealed that natural knockout mice for Art2.a (C57BL/6) or Art2.b (NZW) were resistant to NAD-mediated apoptosis. Labeling with [P-32]NAD revealed strong cell surface ART activity on T cells of C57BL/6 and little if any activity on cells of NZW mice. T cells of (C57BL/6 x NZW)F-1 animals showed strong cell surface ART activity and were very sensitive to NAD-induced apoptosis. As in BALB/c T cells, ART2-specific antisera blocked cell surface ART activity and apoptosis in (C57BL/6 x NZW)F-1 T cells. The fact that T cells of F-1 animals are sensitive to rapid NAD-induced apoptosis suggests that this effectrequires the complementation of (at least) two genetic components. We propose that one of these is cell surface ART2.2 activity (defective in the NZWparent), the other a downstream effector of ADP-ribosylation (defective inthe C57BL/6 parent).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 14:14:29