Mice lacking myeloperoxidase are more susceptible to experimental autoimmune encephalomyelitis
Mice lacking myeloperoxidase are more susceptible to experimental autoimmune encephalomyelitis
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DOI：
10.1016/s0165-5728(00)00392-1
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发表时间：
2001-01-01
影响因子：
3.3
通讯作者：
Reynolds, WF
中科院分区：
文献类型：
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作者：
Brennan, ML;Gaur, A;Reynolds, WF
EAE是一种脱髓鞘疾病，可作为多发性硬化症（MS）的动物模型。髓过氧化物酶（MPO）通过其存在于侵入的巨噬细胞中以及通过-463G/A启动子多态性与风险增加的关联而与MS有关。此外，MPO在17q23.1是在基因组扫描中确定为MS易感基因座的区域内。我们在此研究MPO基因敲除（KO）小鼠中EAE的发生率。在野生型小鼠的CNS中，在侵入的巨噬细胞中检测到MPO，然而出乎意料的是，MPO-KO小鼠具有显著增加的EAE发病率：90%的MPO-KO小鼠发展为完全后肢瘫痪，而野生型（WT）同窝出生的小鼠为33%（P
EAE is a demyelinating disease which serves as an animal model for multiple sclerosis (MS). Myeloperoxidase (MPO) has been implicated in MS through its presence in invading macrophages, and by association of a -463G/A promoter polymorphism with increased risk. Also, MPO at 17q23.1 is within a region identified in genome scans as a MS susceptibility locus. We here examine the incidence of EAE in MPO knockout (KO) mice. MPO is detected in invading macrophages in the CNS of wild-type mice, yet unexpectedly, MPO-KO mice have significantly increased incidence of EAE: Ninety percent of MPO-KO mice developed complete hind limb paralysis as compared to 33% of wildtype (WT) littermates (P