Multiple sclerosis (MS) is a common autoimmune disease that targets myelin in the central nervous system (CNS). Multiple genome-wide association studies (GWAS) over the past 10 years have uncovered more than 200 loci that independently contribute to disease pathogenesis. As with many other complex diseases, risk of developing MS is driven by multiple common variants whose biological effects are not immediately clear. Here, we present a historical perspective on the progress made in MS genetics and discuss current work geared towards creating a more complete model that accurately represents the genetic landscape of MS susceptibility. Such a model necessarily includes a better understanding of the individual contributions of each common variant to the cellular phenotypes, and interactions with other genes and with the environment. Future genetic studies in MS will likely focus on the role of rare variants and endophenotypes.

多发性硬化症（MS）是一种常见的自身免疫性疾病，其靶向中枢神经系统（CNS）中的髓磷脂。在过去的十年中，多项全基因组关联研究（GWAS）已发现200多个独立于疾病发病机理的基因座。与许多其他复杂疾病一样，发生MS的风险是由多种常见变体驱动的，这些变体的生物学效应尚不明确。在这里，我们提供了有关MS遗传学进展的历史观点，并讨论了旨在创建一个更完整的模型的当前工作，该模型可以准确地代表MS易感性的遗传状况。这样的模型必然包括对每个共同变体对细胞表型的贡献以及与其他基因以及与环境的相互作用的更好的理解。