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Titolo:
Fas/Fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance
Autore:
Deng, CS; Goluszko, E; Christadoss, P;
Indirizzi:
Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 biol & Immunol, Galveston, TX 77555 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 5, volume: 166, anno: 2001,
pagine: 3458 - 3467
SICI:
0022-1767(20010301)166:5<3458:FLPAAC>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
AUTOIMMUNE MYASTHENIA-GRAVIS; MYELIN BASIC-PROTEIN; COLLAGEN-INDUCED ARTHRITIS; ORAL TOLERANCE; TRANSGENIC MICE; IN-VIVO; LYMPHOPROLIFERATIVE SYNDROME; PREFERENTIAL USAGE; II COLLAGEN; IFN-GAMMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Christadoss, P Univ Texas, Med Branch, Dept Microbiol & Immunol, 301 Univ Blvd, Galveston, TX 77555 USA Univ Texas 301 Univ Blvd Galveston TX USA 77555 X 77555 USA
Citazione:
C.S. Deng et al., "Fas/Fas ligand pathway, apoptosis, and clonal anergy involved in systemic acetylcholine receptor T cell epitope tolerance", J IMMUNOL, 166(5), 2001, pp. 3458-3467

Abstract

The cellular mechanisms of high dose systemic acetylcholine receptor (AChR) T cell epitope, alpha 146-162 peptide-induced tolerance in experimental myasthenia gravis were examined. CD4 cells are the prime target for alpha 146-162 peptide-induced tolerance. The expression of CD69, Fas, and B7.2 molecules on AChR-immune lymphocytes was enhanced within 4-12 h after toleranceinduction. A high dose of alpha 146-162 peptide in IFA failed to suppress T cell proliferation and/or clinical myasthenia gravis in lpr and gld mice deficient in Fas and Fas ligand, respectively. A high dose of alpha 146-162peptide in IFA in AChR-immunized mice induced apoptosis of BV6 cells. Further, reconstitution of IL-2 in vitro-recovered alpha 146-161 peptide tolerized T cell proliferation, IFN-gamma, and IL-10 production, The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the mechanisms of high dose AChR alpha 146-162 peptide-induced tolerance on CD4 cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 15:28:49