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Titolo:
MODULATION OF SUPERANTIGEN-INDUCED T-CELL DELETION BY ANTIBODY ANTI-PGP-1 (CD44)
Autore:
AYROLDI E; CANNARILE L; RICCARDI C;
Indirizzi:
UNIV PERUGIA,INST PHARMACOL,SCH MED,DEPT CLIN MED PATHOL & PHARMACOL I-06100 PERUGIA ITALY
Titolo Testata:
Immunology
fascicolo: 2, volume: 87, anno: 1996,
pagine: 191 - 197
SICI:
0019-2805(1996)87:2<191:MOSTDB>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
MAJOR HISTOCOMPATIBILITY COMPLEX; CLONAL DELETION; ADHESION MOLECULE; HIGH ENDOTHELIUM; TRANSGENIC MICE; SELF-TOLERANCE; SURFACE LIGAND; ENTEROTOXIN-B; RECEPTOR; ACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
E. Ayroldi et al., "MODULATION OF SUPERANTIGEN-INDUCED T-CELL DELETION BY ANTIBODY ANTI-PGP-1 (CD44)", Immunology, 87(2), 1996, pp. 191-197

Abstract

We examined the effects of anti-Pgp-1 (CD44) antibody on the in vitrodeletion of murine CD4 and CD8 single positive T cells induced by Staphylococcal enterotoxin B (SEE). Soluble anti-Pgp-1 antibody enhanced the apoptosis and decreased the proliferation of SEE-responding T cells. In contrast, cross-linked anti-Pgp-1 antibody provided costimulatory signals for the T-cell activation induced by anti-CD3 antibody. Hyaluronic acid (HA), a ligand of Pgp-1, did not affect proliferation and deletion induced by SEE, whereas it mimicked the effects of the cross-linked antibody in anti-CD3-driven proliferation. T-cell Pgp-1 surfaceexpression after 48 hr incubation with SEE was unchanged as compared to unstimulated cells. However, when the memory T cells were established, some V beta 8(+) (SEB-specific) T cells Pgp-1(low) became Pgp-1(high), displaying a bimodal character. Moreover, the Pgp-1 increased expression correlated with an increase of Pgp-1 soluble form in the supernatant. These findings suggested that signals following the triggeringof the Pgp-1 molecule are important in controlling T-cell survival.

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Documento generato il 02/12/20 alle ore 14:46:27