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Titolo:
Absence of IFN-gamma or IL-12 has different effects on experimental myasthenia gravis in C57BL/6 mice
Autore:
Karachunski, PI; Ostlie, NS; Monfardini, C; Conti-Fine, BM;
Indirizzi:
Univ Minnesota, Dept Biochem Mol Biol & Biophys, St Paul, MN 55108 USA Univ Minnesota St Paul MN USA 55108 Biol & Biophys, St Paul, MN 55108 USA Univ Minnesota, Sch Med, Dept Pharmacol, Minneapolis, MN 55455 USA Univ Minnesota Minneapolis MN USA 55455 rmacol, Minneapolis, MN 55455 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 10, volume: 164, anno: 2000,
pagine: 5236 - 5244
SICI:
0022-1767(20000515)164:10<5236:AOIOIH>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
MUSCLE ACETYLCHOLINE-RECEPTOR; EXPERIMENTAL AUTOIMMUNE UVEITIS; PROGRESSIVE MULTIPLE-SCLEROSIS; T-EPITOPE SEQUENCES; INTERFERON-GAMMA; TGF-BETA; CELL SUBSETS; NOD MICE; EXPERIMENTAL COLITIS; ALPHA-SUBUNIT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
72
Recensione:
Indirizzi per estratti:
Indirizzo: Conti-Fine, BM Univ Minnesota, Dept Biochem Mol Biol & Biophys, 1479 Gortner Ave, St Paul, MN 55108 USA Univ Minnesota 1479 Gortner Ave St Paul MN USA 55108 08 USA
Citazione:
P.I. Karachunski et al., "Absence of IFN-gamma or IL-12 has different effects on experimental myasthenia gravis in C57BL/6 mice", J IMMUNOL, 164(10), 2000, pp. 5236-5244

Abstract

Immunization with acetylcholine receptor (AChR) causes experimental myasthenia gravis (EMG), Th1 cells facilitate EMG development. IFN-gamma and IL-12 induce Th1 responses: we investigated whether these cytokines are necessary for EMG development. We immunized wild-type (WT) C57BL/6 mice and IFN-gamma and IL-12 knockout mutants (IFN-gamma(-/-), IL-12(-/-)) with Torpedo AChR (TAChR), WT and IFN-gamma(-/-) mice developed EMG with similar frequency, IL-12(-/-)mice were resistant to EMG. All strains synthesized anti-AChR Ab that were not IgM or IgE, WT mice had anti-AChR IgG1, IgG2b, and IgG2c, IFN-gamma(-/-) mice had significantly less IgG2c, and IL-12(-/-) mice less IgG2b and IgG2c. All mice had IgG bound to muscle synapses, but only WT and IFN-gamma(-/-) mice had complement; WT mice had both IgG2b and IgG2c, IFN-gamma(-/-) only IgG2b, and IL-12(-/-) neither IgG2b nor IgG2c. CD4(+) cells from all AChR-immunized mice proliferated in response to AChR and recognized similar epitopes, After stimulation with TAChR, CD4(+) cells from IFN-gamma(-/-) mice secreted less IL-2 and similar amounts of IL-4 and IL-10 as WTmice. CD4(+) cells from IL-12(-/-) mice secreted less IFN-gamma, but more IL-4 and IL-10 than WT mice, suggesting that they developed a stronger Th2 response to TAChR, The EMG resistance of IL-12(-/-) mice is likely due to both reduction of anti-TAChR Ab that bind complement and sensitization of modulatory Th2 cells. The reduced Th1 function of IFN-gamma(-/-) mice does not suffice to reduce all complement-fixing IgG subclasses, perhaps because as in WT mice a protective Th2 response is missing.

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Documento generato il 04/12/20 alle ore 01:04:57