Hamann Isabell, Zipp Frauke, Infante-Duarte Carmen
Cecilie Vogt Clinic for Neurology in the Helios-Klinikum Berlin-Buch (HKBB), Charité - Universitätsmedizin Berlin, Germany.
J Neurol Sci. 2008 Nov 15;274(1-2):31-8. doi: 10.1016/j.jns.2008.07.005. Epub 2008 Aug 15.
Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) that is initiated and maintained by continuous migration of inflammatory immune cells from the periphery into the target organ. However, in autoimmunity, migration of immune cells is not only involved in the pathogenesis but also in the down-modulation of the autoimmune attack, which is probably mediated by the infiltration of certain regulatory immune cell populations inside the affected organs. The migratory activity of both proinflammatory and regulatory leucocytes is controlled by chemokines and their receptors. Thus, targeting the directed migration of immune cells and regulating leukocyte trafficking across the blood-brain barrier (BBB) by means of modulation of chemokine signaling receptors might open up new therapeutic avenues not only for MS but also for other autoimmune diseases. In this review we summarize the chemotactic signaling pathways known to be involved in neuroinflammation to date and the viability of these pathways as targets for therapeutic strategies.
多发性硬化症（MS）是一种中枢神经系统（CNS）的自身免疫性疾病，由炎症免疫细胞从外周持续迁移至靶器官引发并维持。然而，在自身免疫中，免疫细胞的迁移不仅参与发病机制，还参与自身免疫攻击的下调，这可能是由受影响器官内某些调节性免疫细胞群体的浸润介导的。促炎和调节性白细胞的迁移活性受趋化因子及其受体控制。因此，通过调节趋化因子信号受体来靶向免疫细胞的定向迁移并调节白细胞穿越血脑屏障（BBB）的运输，可能不仅为MS，也为其他自身免疫性疾病开辟新的治疗途径。在本综述中，我们总结了迄今为止已知参与神经炎症的趋化信号通路以及这些通路作为治疗策略靶点的可行性。
