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Titolo:
Suppression of experimental myasthenia gravis, a B cell-mediated autoimmune disease, by blockade of IL-18
Autore:
Im, SH; Barchan, D; Maiti, PK; Raveh, L; Souroujon, MC; Fuchs, S;
Indirizzi:
Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel Weizmann Inst Sci Rehovot Israel IL-76100 unol, IL-76100 Rehovot, Israel Open Univ, IL-61392 Tel Aviv, Israel Open Univ Tel Aviv Israel IL-61392Open Univ, IL-61392 Tel Aviv, Israel Israel Inst Biol Res, IL-74100 Ness Ziona, Israel Israel Inst Biol Res Ness Ziona Israel IL-74100 74100 Ness Ziona, Israel
Titolo Testata:
FASEB JOURNAL
fascicolo: 12, volume: 15, anno: 2001,
pagine: 2140 - 2148
SICI:
0892-6638(200110)15:12<2140:SOEMGA>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERLEUKIN-1-BETA CONVERTING-ENZYME; ALKALINE-PHOSPHATASE ACTIVITY; ACETYLCHOLINE-RECEPTOR; IFN-GAMMA; CD40 LIGAND; INTERFERON-GAMMA; MONOCLONAL-ANTIBODIES; RECOMBINANT FRAGMENT; NASAL TOLERANCE; EXPRESSION;
Keywords:
autoimmunity; interleukin 18; cytokines and costimulatory factors; immunotherapy; MG;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Fuchs, S Weizmann Inst Sci, Dept Immunol, Wolfson Bldg,Room 404, IL-76100 Rehovot, Israel Weizmann Inst Sci Wolfson Bldg,Room 404 Rehovot Israel IL-76100
Citazione:
S.H. Im et al., "Suppression of experimental myasthenia gravis, a B cell-mediated autoimmune disease, by blockade of IL-18", FASEB J, 15(12), 2001, pp. 2140-2148

Abstract

Interleukin-18 (IL-18) is a pleiotropic proinflammatory cytokine that plays an important role in interferon gamma (IFN-gamma) production and IL-12-driven Th1 phenotype polarization. Increased expression of IL-18 has been observed in several autoimmune diseases. In this study we have analyzed the role of IL-18 in an antibody-mediated autoimmune disease and elucidated the mechanisms involved in disease suppression mediated by blockade of IL-18, using experimental autoimmune myasthenia gravis (EAMG) as a model. EAMG is a T cell-regulated, antibody-mediated autoimmune disease in which the nicotinic acetylcholine receptor (AChR) is the major autoantigen. Th1- and Th2-type responses are both implicated in EAMG development. We show that treatmentby anti-IL-18 during ongoing EAMG suppresses disease progression. The protective effect can be adoptively transferred to naive recipients and is mediated by increased levels of the immunosuppressive Th3-type cytokine TGF-beta and decreased AChR-specific Th1-type cellular responses. Suppression of EAMG is accompanied by down-regulation of the costimulatory factor CD40L andup-regulation of CTLA-4, a key negative immunomodulator. Our results suggest that IL-18 blockade may potentially be applied for immunointervention inmyasthenia gravis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 01:57:30