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Titolo:
PREVENTION OF EXPERIMENTAL MYASTHENIA-GRAVIS BY NASAL ADMINISTRATION OF SYNTHETIC ACETYLCHOLINE-RECEPTOR-T EPITOPE SEQUENCES
Autore:
KARACHUNSKI PI; OSTLIE NS; OKITA DK; CONTIFINE BM;
Indirizzi:
UNIV MINNESOTA,DEPT BIOCHEM,COLL BIOL SCI,1479 GORTNER AVE ST PAUL MN55108 UNIV MINNESOTA,DEPT BIOCHEM,COLL BIOL SCI ST PAUL MN 55108 UNIV MINNESOTA,SCH MED,DEPT PHARMACOL MINNEAPOLIS MN 55455
Titolo Testata:
The Journal of clinical investigation
fascicolo: 12, volume: 100, anno: 1997,
pagine: 3027 - 3035
SICI:
0021-9738(1997)100:12<3027:POEMBN>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; ORAL TOLERANCE; IMMUNE-RESPONSES; MESSENGER-RNA; CELL EPITOPES; CD4(+) CELLS; IFN-GAMMA; TGF-BETA; SUPPRESSION;
Keywords:
ACETYLCHOLINE RECEPTOR; AUTOIMMUNITY; MICE; NASAL TOLERANCE; T CELLS;
Tipo documento:
Article
Natura:
Periodico
Citazioni:
49
Recensione:
Indirizzi per estratti:
Citazione:
P.I. Karachunski et al., "PREVENTION OF EXPERIMENTAL MYASTHENIA-GRAVIS BY NASAL ADMINISTRATION OF SYNTHETIC ACETYLCHOLINE-RECEPTOR-T EPITOPE SEQUENCES", The Journal of clinical investigation, 100(12), 1997, pp. 3027-3035

Abstract

T cell tolerization prevents and improves T cell-mediated experimental autoimmune diseases. We investigated here whether similar approachescould be used for antibody (Ab)-mediated autoimmune diseases, Myasthenia gravis, caused by IgG Ab against muscle acetylcholine receptor (AChR), is perhaps the best characterized of them. We used an animal model, experimental myasthenia gravis induced in C57Bl/6 mice by immunization with Torpedo acetylcholine receptor (TAChR), to demonstrate that nasal administration of synthetic sequences of the TAChR alpha-subunit-forming epitopes recognized by anti-TAChR CD4(+) T helper cells (residues alpha 150-169, alpha 181-200, and alpha 360-378), given before andduring immunization with TAChR, causes decreased CD4(+) responsiveness to those epitopes and to TAChR, reduced synthesis of anti-TAChR Ab, and prevented experimental myasthenia gravis. These effects were not induced by nasal administration of synthetic epitopes of diphtheria toxin. Secretion of IL-2, 1L-4, and IL-10 by spleen T cells from TAChR immunized mice, in response to challenge with TAChR in vitro, indicated that in sham-tolerized mice only Th1 cells responded to TAChR, while peptide-treated mice had also an AChR-specific Th2 response. The TAChR peptide treatment induced also in vitro anergy to the TAChR of the spleen T cells, which was reversed by IL-2.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 09:25:33