多发性硬化（multiple sclerosis，MS）是一种慢性疾病，具有高潜在致残率，伴随着相当大的社会影响和经济后果。SSeCKS介导星形胶质细胞炎性激活在MS过程中发挥重要作用。我们先前的研究发现：与SSeCKS相互作用的HSPA12B参与炎症诱导的星形胶质细胞的激活和迁移过程。本课题拟通过MS动物模型EAE，研究SSeCKS和HSPA12B在MS炎症和星形胶质细胞活化过程中的表达及相互作用；通过研究星形胶质细胞炎性活化模型，阐明HSPA12B通过与SSeCKS不同位点的相互结合，调节SSeCKS的活性，从而调控星形胶质细胞炎性激活；通过星形胶质细胞与少突胶质细胞共培养，阐明两者相互作用对髓鞘形成相关蛋白表达的影响，从而探讨两者在MS脱髓鞘过程中的作用和分子机制，籍以为MS的预防和治疗提供新的方法。

Multiple sclerosis (MS) is a chronic and potentially highly disabling disorder with considerable social impact and economic consequences. Inflammatory activation of astrocyte mediated by SSeCKS played an important role in multiple sclerosis. Our previous studies had found that HSPA12B interacted with SSeCKS involved in astrocyte activation and migration induced by inflammation. In this study, EAE, the common animal model of MS was used to study the expression and interaction between SSeCKS and HSPA12B during inflammation and astrocyte activation in MS. To clarify the binding sites of SSeCKS and HSPA12B which regulated the activity of SSeCKS and the inflammatory activation of astrocyte , the inflammatory activation model of astrocyte was established. By co-culturing of astrocytes and oligodendrocytes to demonstrate the impact of the interaction of SSeCKS and HSPA12B to the molecul related to myelination. Finally, to clarify the molecular mechanisms of demyelinating process in MS, and to provide a new way for the prevention and treatment of MS.