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Titolo:
Transgenic expression of IL-10 in T cells facilitates development of experimental myasthenia gravis
Autore:
Ostlie, NS; Karachunski, PI; Wang, W; Monfardini, C; Kronenberg, M; 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 La Jolla Inst Allergy & Immunol, Div Dev Immunol, San Diego, CA 92121 USA La Jolla Inst Allergy & Immunol San Diego CA USA 92121 iego, CA 92121 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: 8, volume: 166, anno: 2001,
pagine: 4853 - 4862
SICI:
0022-1767(20010415)166:8<4853:TEOIIT>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
MUSCLE ACETYLCHOLINE-RECEPTOR; SYSTEMIC-LUPUS-ERYTHEMATOSUS; B-LYMPHOCYTES DIFFERENTIATE; NONOBESE DIABETIC MICE; IFN-GAMMA; TGF-BETA; EPITOPE SEQUENCES; HUMAN INTERLEUKIN-10; INTERFERON-GAMMA; CYTOKINES INDUCE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
82
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:
N.S. Ostlie et al., "Transgenic expression of IL-10 in T cells facilitates development of experimental myasthenia gravis", J IMMUNOL, 166(8), 2001, pp. 4853-4862

Abstract

Ab to the acetylcholine receptor (AChR) cause experimental myasthenia gravis (EMG). Th1 cytokines facilitate EMG, whereas Th2 cytokines might be protective. IL-10 inhibits Th1 responses but facilitates B cell proliferation and Ig production. We examined the role of IL-10 in EMG by using wild-type (WT) C57BL/6 mice and transgenic (TG) C57BL/6 mice that express IL-10 under control of the IL-2 promoter. We immunized the mice with doses of AChR thatcause EMG in WT mice or with low doses ineffective at causing EMG in WT mice. After low-dose AChR immunization, WT mice did not develop EMG and had very little anti-AChR serum Ab, which were mainly IgG1, whereas TG mice developed EMG and had higher levels of anti-AChR serum Ab, which were mainly IgG2, in addition to IgG1. At the higher doses, TG mice developed EMG earlierand more frequently than WT mice and had more serum anti-AChR Ab. Both strains had similar relative serum concentrations of anti-AChR IgG subclasses and IgG and complement at the muscle synapses. CD8(+)-depleted splenocytes from all AChR-immunized mice proliferated in the presence of AChR and recognized a similar epitope repertoire. CD8(+)-depleted splenocytes from AChR-immunized TG mice stimulated in vitro with AChR secreted significantly more IL-10, but less of the prototypic Th1 cytokine IFN-gamma, than those from WT mice. They secreted comparable amounts of IL-4 and slightly but not significantly reduced amounts of IL-2. This suggests that TG mice had reduced activation of anti-Torpedo AChR Th1 cells, but increased anti-AChR Ab synthesis, that likely resulted from IL-10-mediated stimulation of anti-AChR B cells. Thus, EMG development is not strictly dependent on Th1 cell activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 08:59:05