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Breast regression protein-39 is not required for experimental autoimmune encephalomyelitis induction

机译:实验性自身免疫性脑脊髓炎的诱导不需要乳房消退蛋白39

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摘要

Increasing evidence points to a role for chitinase 3-like 1 (CHI3L1) in multiple sclerosis (MS). Here, we aimed to explore the potential involvement of CHI3L1 in the animal model of MS, experimental autoimmune encephalomyelitis (EAE). EAE was induced by immunization with MOG(35-55) peptide in wild-type (WT) and knock-out (KO) mice for breast regression protein 39 (BRP-39), the mouse homologue of human CHI3L1. Immunological responses in splenocytes were assessed by means of polyclonal and antigen-specific proliferation assays. Central nervous system. pathology and chitinase gene expression were also investigated. BRP-39 expression was increased in WT MOG(35-55)-immunized mice compared to saline-immunized controls. No differences were found between WT and BRP-39 KO mice regarding EAE clinical course, day of disease onset, mortality rate, splenocyte proliferative responses or histopathological findings. These results do not support a role of BRP-39 in the pathogenesis of EAE. (C) 2015 Elsevier Inc. All rights reserved.
机译:越来越多的证据表明几丁质酶3样1(CHI3L1)在多发性硬化症(MS)中的作用。在这里,我们旨在探讨CHI3L1在MS动物模型中的作用,即实验性自身免疫性脑脊髓炎(EAE)。通过在野生型(WT)和基因敲除(KO)小鼠中用MOG(35-55)肽免疫接种人乳腺回归蛋白39(BRP-39)(人CHI3L1的小鼠同源物)来诱导EAE。通过多克隆和抗原特异性增殖测定法评估脾细胞中的免疫反应。中枢神经系统。还研究了病理学和几丁质酶基因表达。与盐水免疫对照组相比,WT MOG(35-55)免疫小鼠中BRP-39表达增加。 WT和BRP-39 KO小鼠在EAE临床病程,发病日期,死亡率,脾细胞增殖反应或组织病理学发现方面无差异。这些结果不支持BRP-39在EAE发病机理中的作用。 (C)2015 Elsevier Inc.保留所有权利。

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