Regulation of experimental autoimmune encephalomyelitis by chemokines and chemokine receptors
Regulation of experimental autoimmune encephalomyelitis by chemokines and chemokine receptors
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DOI：
10.1385/ir:25:2:167
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发表时间：
2002-01-01
影响因子：
4.4
通讯作者：
Karpus, WJ
中科院分区：
文献类型：
--
作者：
Elhofy, A;Kennedy, KJ;Karpus, WJ
实验性自身免疫性脑脊髓炎(EAE)是一种T细胞介导的中枢神经系统(CNS)脱髓鞘疾病，是多发性硬化(MS)的模型。对这种模型的发病机制的洞察可能有助于科学家了解人类疾病，并有助于理性的药物发现。在这篇综述中，我们总结了趋化因子和趋化因子受体在疾病发病机制中的作用，并提出了导致脱髓鞘和随后的临床疾病表现的事件途径。
Experimental autoimmune encephalomyelitis (EAE) is a T cell mediated demyelinating disease of the central nervous system (CNS) that serves as a model for multiple sclerosis (MS). Insights into the pathogenesis of this model may help scientists understand the human disease and aid in rational drug discovery. In this review we summarize the role of chemokines and chemokine receptors in disease pathogenesis and suggest a pathway of events that leads to demyelination and subsequent clinical disease manifestation.