Proudfoot Amanda E I, de Souza Adriano Luís Soares, Muzio Valeria
Merck Serono Geneva Research Centre, 9 chemin des Mines, Geneva, Switzerland.
J Neuroimmunol. 2008 Jul 31;198(1-2):27-30. doi: 10.1016/j.jneuroim.2008.04.007. Epub 2008 Jun 11.
Multiple sclerosis is believed to be an autoimmune disease with an end-point of neuro-degeneration, but in which inflammation plays a predominant role. Therefore therapies which target inhibition of the excessive recruitment of leukocytes into the central nervous system (CNS) are actively sought after by medical research. Drug discovery relies heavily on animal models used for such research, called Experimental Autoimmune Encephalomyelitis (EAE). Several chemokines and their receptors have been shown to play a role in this recruitment into the CNS, and we have investigated several strategies which antagonize this system in EAE models. We will discuss these strategies and their successes and failures to prevent disease symptoms and the insights they have provided.
多发性硬化症被认为是一种以神经退行性变作为终点的自身免疫性疾病,不过炎症在其中起着主要作用。因此,医学研究积极探寻旨在抑制白细胞过度募集进入中枢神经系统(CNS)的疗法。药物研发在很大程度上依赖于用于此类研究的动物模型,即实验性自身免疫性脑脊髓炎(EAE)。已有多种趋化因子及其受体被证明在这种向中枢神经系统的募集过程中发挥作用,并且我们已经在EAE模型中研究了几种拮抗该系统的策略。我们将讨论这些策略以及它们在预防疾病症状方面的成败情况,以及它们所提供的见解。