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首页> 外文期刊>Journal of Clinical Medicine >Can the Fact That Myelin Proteins Are Old and Break down Explain the Origin of Multiple Sclerosis in Some People?
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Can the Fact That Myelin Proteins Are Old and Break down Explain the Origin of Multiple Sclerosis in Some People?

机译：髓磷脂蛋白老化并分解的事实能否解释某些人的多发性硬化症起源？

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Recent discoveries may change the way that multiple sclerosis (MS) is viewed, particularly with regard to the reasons for the untoward immune response. The fact that myelin proteins are long-lived, and that by the time we are adults, they are extensively degraded, alters our perspective on the reasons for the onset of autoimmunity and the origin of MS. For example, myelin basic protein (MBP) from every human brain past the age of 20 years, is so greatly modified, that it is effectively a different protein from the one that was laid down in childhood. Since only a subset of people with such degraded MBP develop MS, a focus on understanding the mechanism of immune responses to central nervous system (CNS) antigens and cerebral immune tolerance appear to be worthwhile avenues to explore. In accord with this, it will be productive to examine why all people, whose brains contain large quantities of a “foreign antigen”, do not develop MS. Importantly for the potential causation of MS, MBP from MS patients breaks down differently from the MBP in aged controls. If the novel structures formed in these MS-specific regions are particularly antigenic, it could help explain the origin of MS. If verified, these findings could provide an avenue for the rational synthesis of drugs to prevent and treat MS.
机译：最近的发现可能会改变观察多发性硬化症（MS）的方式，特别是在免疫反应不良的原因方面。髓鞘蛋白寿命长，并且在我们成年时已经广泛降解，这一事实改变了我们对自身免疫性发作原因和MS起源的看法。例如，超过20岁的人脑中的髓磷脂碱性蛋白（MBP）进行了如此巨大的修饰，以至于它实际上是与童年时期沉积的蛋白不同的蛋白。由于只有一部分患有这种MBP降解的人发展为MS，因此集中精力了解对中枢神经系统（CNS）抗原的免疫反应机制和脑部免疫耐受性似乎是值得探索的途径。据此，研究为什么所有人的大脑中都含有大量的“外源抗原”将不会发展为MS将是有益的。重要的是，对于MS的潜在病因，MS患者的MBP分解与老年对照组的MBP有所不同。如果在这些MS特异性区域中形成的新结构特别具有抗原性，则可以帮助解释MS的起源。如果得到证实，这些发现将为合理合成预防和治疗MS的药物提供一条途径。

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