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表达白细胞介素-4的质粒DNA可抑制DBA/1 J乳鼠中2型呼肠孤病毒引发的自身免疫性胰岛炎。

Interleukin-4-expressing plasmid DNA inhibits reovirus type-2-triggered autoimmune insulitis in DBA/1 J suckling mice.

作者信息

Hayashi T, Yasutomi Y, Hasegawa K, Sasaki Y, Onodera T

机构信息

Laboratory of Veterinary Pathology, Yamaguchi University, Yamaguchi, Japan.

出版信息

Int J Exp Pathol. 2003 Apr;84(2):101-6. doi: 10.1046/j.1365-2613.2003.00341.x.

Abstract

In this study we have examined the effect of systemic administration of T helper (Th) 2 cytokines on reovirus type-2 (Reo-2)-triggered Th1-mediated autoimmune insulitis with impaired glucose tolerance (IGT) in DBA/1J suckling mice. We have demonstrated clearly that the systemic administration of both interleukin (IL)-4-expressing plasmid DNA (pIL-4) and recombinant IL-4 (rIL-4) inhibited the development of insulitis with IGT in a dose dependent manner as compared to untreated groups in Reo-2-infected DBA/1J suckling mice. The inhibitory effects of IL-4 on the development of insulitis with IGT and the advantages of pIL-4 as compared to rIL-4 in this model are discussed.

摘要

在本研究中,我们检测了全身性给予辅助性T细胞(Th)2细胞因子对呼肠孤病毒2型(Reo-2)引发的、伴有葡萄糖耐量受损(IGT)的Th1介导的自身免疫性胰岛炎在DBA/1J乳鼠中的影响。我们已明确证明,与未处理组相比,在感染Reo-2的DBA/1J乳鼠中,全身性给予表达白细胞介素(IL)-4的质粒DNA(pIL-4)和重组IL-4(rIL-4)均以剂量依赖性方式抑制了伴有IGT的胰岛炎的发展。本文讨论了IL-4对伴有IGT的胰岛炎发展的抑制作用以及在此模型中pIL-4相对于rIL-4的优势。

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Plasmid encoding interferon-gamma exacerbates reovirus type-2-induced diabetes in DBA/1 suckling mice.
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