Cutting edge:: Oral type I IFN-τ promotes a Th2 bias and enhances suppression of autoimmune encephalomyelitis by oral glatiramer acetate
Cutting edge:: Oral type I IFN-τ promotes a Th2 bias and enhances suppression of autoimmune encephalomyelitis by oral glatiramer acetate
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DOI:
10.4049/jimmunol.169.5.2231
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发表时间:
2002-09-01
影响因子:
4.4
通讯作者:
Zamvil, SS
中科院分区:
文献类型:
--
作者:
Soos, JM;Stüve, O;Zamvil, SS
IFN-tau, a novel type I IFN that possesses immunomodulatory properties, lacks toxicity normally associated with other type I IFNs. We examined the effects of oral IFN-tau alone and in combination with oral glatiramer acetate in experimental allergic encephalomyelitis (EAE). By comparison of oral administration of IFN-alpha, -beta, and -tau to myelin basic protein-specific TCR-transgenic mice, we demonstrate these type I IFNs promote secretion of the Th2 cytokine IL-10 with similar efficiency. Whereas IFN-alpha and -beta induced IFN-gamma secretion, a Th1 cytokine, IFN-tau did not. Oral IFN-tau alone suppressed EAE. When suboptimal doses were administered orally in combination to wild-type mice, IFN-tau and glatiramer acetate had a synergistic beneficial effect in suppression of EAE. This combination was associated with TGF-beta secretion and enhanced IL-10 production. Thus, IFN-tau is a potential candidate for use as a single agent or in combination therapy for multiple sclerosis.