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首页> 外文期刊>Nature immunology >Activated leukocyte cell adhesion molecule promotes leukocyte trafficking into the central nervous system
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Activated leukocyte cell adhesion molecule promotes leukocyte trafficking into the central nervous system

机译：活化的白细胞粘附分子促进白细胞向中枢神经系统的运输

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摘要

Adhesion molecules of the immunoglobulin superfamily are crucial effectors of leukocyte trafficking into the central nervous system. Using a lipid raft-based proteomic approach, we identified ALCAM as an adhesion molecule involved in leukocyte migration across the blood-brain barrier (BBB). ALCAM expressed on BBB endothelium localized together with CD6 on leukocytes and with BBB endothelium transmigratory cups. ALCAM expression on BBB cells was upregulated in active multiple sclerosis and experimental autoimmune encephalomyelitis lesions. Moreover, ALCAM blockade restricted the transmigration of CD4(+) lymphocytes and monocytes across BBB endothelium in vitro and in vivo and reduced the severity and delayed the time of onset of experimental autoimmune encephalomyelitis. Our findings indicate an important function for ALCAM in the recruitment of leukocytes into the brain and identify ALCAM as a potential target for the therapeutic dampening of neuroinflammation.
机译：免疫球蛋白超家族的粘附分子是白细胞转运到中枢神经系统的关键效应子。使用基于脂质筏的蛋白质组学方法，我们将ALCAM确定为参与白血球穿过血脑屏障（BBB）迁移的粘附分子。在BBB内皮上表达的ALCAM与CD6一起位于白细胞和BBB内皮转运杯上。在活动性多发性硬化症和实验性自身免疫性脑脊髓炎病变中，BBB细胞上的ALCAM表达上调。此外，ALCAM阻断在体外和体内都限制了CD4（+）淋巴细胞和单核细胞跨BBB内皮的迁移，降低了严重程度并延缓了实验性自身免疫性脑脊髓炎的发作时间。我们的发现表明，ALCAM在将白细胞募集到大脑中具有重要作用，并将ALCAM鉴定为治疗性神经炎症缓解的潜在靶标。

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