Oral treatment with laquinimod augments regulatory T-cells and brain-derived neurotrophic factor expression and reduces injury in the CNS of mice with experimental autoimmune encephalomyelitis

被引：69

作者：

Aharoni, Rina ^{[1
]}

Saada, Ravit ^{[1
]}

Eilam, Raya ^{[2
]}

Hayardeny, Liat ^{[3
]}

Sela, Michael ^{[1
]}

Arnon, Ruth ^{[1
]}

机构：

[1] Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel

[2] Weizmann Inst Sci, Dept Vet Resources, IL-76100 Rehovot, Israel

[3] Teva Pharmaceut Ind, Global Innovat R&D, Pharmacol Unit, Netanya, Israel

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2012年 / 251卷 / 1-2期

关键词：

Multiple sclerosis; Experimental autoimmune encephalomyelitis (EAE); T-regulatory cells; Brain derived neurotrophic factor (BDNF); Neuroprotection; Laquinimod; REMITTING MULTIPLE-SCLEROSIS; NEUROPROTECTION; IMMUNE; PHASE; MS;

D O I：

10.1016/j.jneuroim.2012.06.005

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

Laquinimod is an orally active molecule that showed efficacy in clinical trials in multiple sclerosis. We studied its effects in the CNS, when administered by therapeutic regimen to mice inflicted with experimental autoimmune encephalomyelitis (EAE). Laquinimod reduced clinical and inflammatory manifestations and elevated the prevalence of T-regulatory cells in the brain. In untreated mice, in the chronic disease stage, brain derived neurotrophic factor (BDNF) expression was impaired. Laquinimod treatment restored BDNF expression to its level in healthy controls. Furthermore, CNS injury, manifested by astrogliosis, demyelination and axonal damages, was significantly reduced following laquinimod treatment, indicating its immunomodulatory and neuroprotective activity. (C) 2012 Elsevier B.V. All rights reserved.

引用

页码：14 / 24

页数：11

共 26 条

[1]

The immunomodulator glatiramer acetate augments the expression of neurotrophic factors in brains of experimental autoimmune encephalomyelitis mice [J].