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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Laquinimod (ABR-215062) suppresses the development of experimental autoimmune encephalomyelitis, modulates the Th1/Th2 balance and induces the Th3 cytokine TGF-beta in Lewis rats.
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Laquinimod (ABR-215062) suppresses the development of experimental autoimmune encephalomyelitis, modulates the Th1/Th2 balance and induces the Th3 cytokine TGF-beta in Lewis rats.

机译：拉喹莫德（ABR-215062）抑制Lewis鼠实验性自身免疫性脑脊髓炎的发展，调节Th1 / Th2平衡并诱导Th3细胞因子TGF-β。

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摘要

The new orally active drug laquinimod (ABR-215062) was evaluated in experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. EAE shares important immunological and clinical features with multiple sclerosis (MS). Doses of 16, 1.6 and 0.16 mg/kg/day laquinimod dose-dependently inhibited disease and showed better disease inhibitory effects as compared to roquinimex (Linomide). Furthermore, laquinimod inhibited the inflammation of both CD4(+) T cells and macrophages into central nervous tissues, i.e. the spinal cord. It also changed the cytokine balance in favour of T(H)2/T(H)3 cytokines IL-4, IL-10 and TGF-beta. Laquinimod therefore represents a new orally active immunoregulatory drug without general immunosuppressive properties with a potential for the treatment of severe autoimmune diseases like MS.
机译：在Lewis大鼠的实验性自身免疫性脑脊髓炎（EAE）中评估了新的口服活性药物拉喹莫德（ABR-215062）。 EAE与多发性硬化症（MS）具有重要的免疫学和临床特征。与roquinimex（Linomide）相比，拉喹莫德的剂量为16、1.6和0.16 mg / kg / day，剂量依赖性地抑制疾病，并显示出更好的疾病抑制作用。此外，拉喹莫德抑制CD4（+）T细胞和巨噬细胞进入中枢神经组织即脊髓的炎症。它还改变了细胞因子平衡，有利于T（H）2 / T（H）3细胞因子IL-4，IL-10和TGF-beta。因此，拉喹莫德代表了一种新的口服活性免疫调节药物，没有一般的免疫抑制特性，具有治疗严重的自身免疫性疾病（如MS）的潜力。

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