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Titolo:
Interleukin 10 aggravates experimental autoimmune myasthenia gravis through inducing Th2 and B cell responses to AChR
Autore:
Zhang, GX; Xiao, BG; Yu, LY; van der Meide, PH; Link, H;
Indirizzi:
Huddinge Univ Hosp, Karolinska Inst, Div Neurol, Expt Neuroimmunol Unit, S-14186 Huddinge, Sweden Huddinge Univ Hosp Huddinge Sweden S-14186 nit, S-14186 Huddinge, Sweden Univ Utrecht, Cent Anim Lab, Utrecht, Netherlands Univ Utrecht Utrecht Netherlands t, Cent Anim Lab, Utrecht, Netherlands
Titolo Testata:
JOURNAL OF NEUROIMMUNOLOGY
fascicolo: 1, volume: 113, anno: 2001,
pagine: 10 - 18
SICI:
0165-5728(20010201)113:1<10:I1AEAM>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYSTEMIC-LUPUS-ERYTHEMATOSUS; MESSENGER-RNA EXPRESSION; GROWTH-FACTOR-BETA; ACETYLCHOLINE-RECEPTOR; INTERFERON-GAMMA; MULTIPLE-SCLEROSIS; IFN-GAMMA; T-CELLS; INDUCTION; MICE;
Keywords:
myasthenia gravis; IL-10; autoimmunity; cytokine; antibody;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Zhang, GX Univ Penn, Div Neurol, 464 Stemmler Hall,36th & Hamilton Walk, Philadelphia, PA 19104 USA Univ Penn 464 Stemmler Hall,36th & Hamilton Walk Philadelphia PA USA 19104
Citazione:
G.X. Zhang et al., "Interleukin 10 aggravates experimental autoimmune myasthenia gravis through inducing Th2 and B cell responses to AChR", J NEUROIMM, 113(1), 2001, pp. 10-18

Abstract

The damage of acetylcholine receptor (AChR) at neuromuscular junctions of experimental autoimmune myasthenia gravis (EAMG), an animal model of human MG, is mediated by B cells which require T cell help. The Th2 associated cytokine IL-10 suppresses production of cytokines released by Th1 cells and is considered for treatment of human autoimmune diseases. To evaluate the role of IL-10 in EAMG, rhIL-10 was administered daily to Lewis rats by the subcutaneous route starting at the day of immunization and continued for 7 weeks. IL-10 failed to abrogate EAMG at low dose (0.1 or 1 mug/day) and at the dose of 3 mug/day caused earlier onset and aggravated clinical signs of EAMG when compared to EAMG rats injected with PBS only. Although Th1 responses reflected by AChR-induced lymphocyte proliferation and levels of IFN-gamma secreting cells, as well as AChR-induced Th1 cytokine mRNA expression was suppressed, augmented IL-4 mRNA expression and AChR-specific B cell responses may play an important role in the failure of IL-10 to abrogate EAMG. This study implicates a critical precaution in planning immunotherapy of TL-IO in antibody-mediated autoimmune diseases, e.g. MG. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/10/20 alle ore 09:17:49