Department of Neurology, Frenchay Hospital, University of Bristol, UK.
Cell Prolif. 2011 Apr;44 Suppl 1(Suppl 1):35-8. doi: 10.1111/j.1365-2184.2010.00721.x.
Multiple sclerosis (MS) is a common neurological disease and a major cause of disability, particularly affecting young adults. It is characterized by patches of damage occurring throughout the brain and spinal cord, with loss of myelin sheaths - the insulating material around nerve fibres that allows normal conduction of nerve impulses - accompanied by loss of cells that make myelin (oligodendrocytes). In addition, we now know that there is damage to nerve cells (neurones) and their fibres (axons) too, and that this occurs both within these discrete patches and in tissue between them. The cause of MS remains unknown, but an autoimmune reaction against oligodendrocytes and myelin is generally assumed to play a major role, and early acute MS lesions almost invariably show prominent inflammation. Efforts to develop cell therapy in MS have long been directed towards directly implanting cells capable of replacing lost oligodendrocytes and regenerating myelin sheaths. Accordingly, the advent of techniques to generate large numbers of oligodendrocytes from embryonic stem cells appeared a significant step towards new stem cell treatments for MS; while the emerging consensus that adult stem cells from, for example, the bone marrow had far less potential to turn into oligodendrocytes was thought to cast doubt on their potential value in this disease. A number of scientific and medical concerns, not least the risk of tumour formation associated with embryonic stem cells, have however, prevented any possible clinical testing of these cells in patients. More recently, increasing understanding of the complexity of tissue damage in MS has emphasized that successful cell therapy may need to achieve far more than simply offering a source of replacement myelin-forming cells. The many and varied reparative properties of bone marrow-derived (mesenchymal) stem cells may well offer new and attractive possibilities for developing cell-based treatments for this difficult and disabling condition.
多发性硬化症（MS）是一种常见的神经系统疾病，也是导致残疾的主要原因，尤其影响年轻人。其特征是大脑和脊髓中出现多个损伤斑块，导致髓鞘（神经纤维周围的绝缘材料）丧失，同时产生髓鞘的细胞（少突胶质细胞）也会丢失。此外，我们现在知道神经细胞（神经元）及其纤维（轴突）也会受损，这种损伤不仅发生在这些离散斑块内，也发生在它们之间的组织中。MS 的病因仍然未知，但一般认为针对少突胶质细胞和髓鞘的自身免疫反应起主要作用，早期急性 MS 病变几乎总是表现出明显的炎症。长期以来，人们一直致力于开发 MS 的细胞疗法，旨在直接植入能够替代丢失的少突胶质细胞并再生髓鞘的细胞。因此，从胚胎干细胞中大量产生少突胶质细胞的技术的出现，似乎是 MS 新干细胞治疗的重要一步；而新兴的共识是，来自骨髓等的成体干细胞转化为少突胶质细胞的潜力要小得多，这让人对它们在这种疾病中的潜在价值产生了怀疑。然而，许多科学和医学方面的担忧，尤其是与胚胎干细胞相关的肿瘤形成风险，阻止了这些细胞在患者中进行任何可能的临床测试。最近，对 MS 组织损伤复杂性的认识不断加深，强调成功的细胞疗法可能需要实现的远不止提供替代髓鞘形成细胞的来源。骨髓来源（间充质）干细胞的多种修复特性很可能为这种困难和致残疾病的细胞治疗提供新的、有吸引力的可能性。
