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Chemokines Referee Inflammation within the Central Nervous System during Infection and Disease

机译:感染和疾病期间中枢神经系统内趋化因子裁判员的炎症

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The discovery that chemokines and their receptors are expressed by a variety of cell types within the normal adult central nervous system (CNS) has led to an expansion of their repertoire as molecular interfaces between the immune and nervous systems. Thus, CNS chemokines are now divided into those molecules that regulate inflammatory cell migration into the CNS and those that initiate CNS repair from inflammation-mediated tissue damage. Work in our laboratory throughout the past decade has sought to elucidate how chemokines coordinate leukocyte entry and interactions at CNS endothelial barriers, under both homeostatic and inflammatory conditions, and how they promote repair within the CNS parenchyma. These studies have identified several chemokines, including CXCL12 and CXCL10, as critical regulators of leukocyte migration from perivascular locations. CXCL12 additionally plays an essential role in promoting remyelination of injured white matter. In both scenarios we have shown that chemokines serve as molecular links between inflammatory mediators and other effector molecules involved in neuroprotective processes.
机译:趋化因子及其受体在正常成人中枢神经系统(CNS)中由多种细胞类型表达的发现导致其作为免疫系统和神经系统之间分子界面的分子库的扩大。因此,现在将CNS趋化因子分为那些调节炎症细胞向CNS迁移的分子和那些从炎症介导的组织损伤中引发CNS修复的分子。在过去的十年中,我们实验室的工作一直试图阐明趋化因子如何在稳态和炎性条件下协调中枢神经系统内皮屏障中白细胞的进入和相互作用,以及它们如何促进中枢神经实质内的修复。这些研究已经确定了几种趋化因子,包括CXCL12和CXCL10,它们是白细胞从血管周围位置迁移的关键调节剂。 CXCL12在促进受伤的白质的髓鞘再生中也起着至关重要的作用。在这两种情况下,我们都表明趋化因子是炎症介质和参与神经保护过程的其他效应分子之间的分子连接。

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