McQualter Jonathan L, Bernard Claude C A
Monash Immunology and Stem Cell Laboratories, Monash University, Clayton, Victoria, Australia.
J Neurochem. 2007 Jan;100(2):295-306. doi: 10.1111/j.1471-4159.2006.04232.x. Epub 2006 Nov 13.
Multiple sclerosis (MS) is a chronic neurodegenerative disease of the CNS in which an unrelenting attack from the innate and adaptive arms of the immune system results in extensive demyelination, loss of oligodendrocytes and axonal degeneration. This review summarizes advances in the understanding of the cellular and molecular pathways involved in neurodegeneration following autoimmune-mediated inflammation in the CNS. The mechanisms underlying myelin and axonal destruction and the equally important interaction between degenerative and repair mechanisms are discussed. Recent studies have revealed that the failure of CNS regeneration may be in part a result of the presence of myelin-associated growth inhibitory molecules in MS lesions. Successful therapeutic intervention in MS is likely to require suppression of the inflammatory response, in concert with blockade of growth inhibitory molecules and possibly the mobilization or transplantation of stem cells for regeneration.
多发性硬化症（MS）是一种中枢神经系统的慢性神经退行性疾病，免疫系统的固有免疫和适应性免疫分支持续攻击会导致广泛的脱髓鞘、少突胶质细胞丢失和轴突退化。本综述总结了在理解中枢神经系统自身免疫介导的炎症后神经退行性变所涉及的细胞和分子途径方面取得的进展。讨论了髓鞘和轴突破坏的潜在机制以及退化和修复机制之间同样重要的相互作用。最近的研究表明，中枢神经系统再生失败可能部分是由于MS病变中存在髓鞘相关生长抑制分子。成功治疗MS可能需要抑制炎症反应，同时阻断生长抑制分子，并可能动员或移植干细胞进行再生。
