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PSGL-1 is not required for development of experimental autoimmune encephalomyelitis.

机译:实验性自身免疫性脑脊髓炎的发展不需要PSGL-1。

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摘要

Adhesion molecules are essential mediators for lymphocyte trafficking through the blood-brain barrier into the CNS in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the role of the selectin molecules and their ligand, P-selectin glycoprotein-1 (PSGL-1) which mediates tethering and rolling of the leukocytes in demyelinating disease remains controversial. This study demonstrates that mice deficient in PSGL-1 are not significantly different in the development and progression of EAE compared to wild type controls. Our observations suggest that PSGL-1-selectin interactions are redundant and not required for the development of EAE. Our data also indicate that other adhesion molecules are necessary for the initial rolling events leading to leukocyte infiltration into the CNS during EAE.
机译:在多发性硬化症及其动物模型实验性自身免疫性脑脊髓炎(EAE)中,粘附分子是淋巴细胞通过血脑屏障向CNS转运的重要介质。然而,在脱髓鞘疾病中介导白细胞束缚和滚动的选择蛋白分子及其配体P-选择蛋白糖蛋白-1(PSGL-1)的作用仍存在争议。这项研究表明,与野生型对照组相比,PSGL-1缺陷型小鼠在EAE的发生和发展方面没有显着差异。我们的观察结果表明PSGL-1-选择素相互作用是多余的,对于EAE的发展不是必需的。我们的数据还表明,其他的粘附分子对于导致EAE期间白细胞浸入CNS的初始滚动事件是必需的。

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