Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, People's Republic of China; NHC Key Laboratory of Myopia and Related Eye Diseases, Key Laboratory of Myopia and Related Eye Diseases, Chinese Academy of Medical Sciences, Shanghai, People's Republic of China; Shanghai Key Laboratory of Visual Impairment and Restoration, Shanghai, People's Republic of China; State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, People's Republic of China.
Department of Ophthalmology, Zhongshan Hospital, Fudan University, Shanghai, People's Republic of China.
Mol Cell Proteomics. 2024 Jun;23(6):100783. doi: 10.1016/j.mcpro.2024.100783. Epub 2024 May 9.
High myopia is a leading cause of blindness worldwide, among which pathologic myopia, characterized by typical myopic macular degeneration, is the most detrimental. However, its pathogenesis remains largely unknown. Here, using a HuProt array, we first initiated a serological autoantibody profiling of high myopia and identified 18 potential autoantibodies, of which anti-LIMS1 autoantibody was validated by a customized focused microarray. Further subgroup analysis revealed its actual relevance to pathologic myopia, rather than simple high myopia without myopic macular degeneration. Mechanistically, anti-LIMS1 autoantibody predominantly belonged to IgG1/IgG2/IgG3 subclasses. Serum IgG obtained from patients with pathologic myopia could disrupt the barrier function of retinal pigment epithelial cells via cytoskeleton disorganization and tight junction component reduction, and also trigger a pro-inflammatory mediator cascade in retinal pigment epithelial cells, which were all attenuated by depletion of anti-LIMS1 autoantibody. Together, these data uncover a previously unrecognized autoimmune etiology of myopic macular degeneration in pathologic myopia.
高度近视是全球致盲的主要原因之一,其中病理性近视是最具危害性的,其特征为典型的近视性黄斑变性。然而,其发病机制在很大程度上仍不清楚。在这里,我们首次使用 HuProt 芯片,对高度近视进行了血清自身抗体谱分析,鉴定出 18 种潜在的自身抗体,其中抗 LIMS1 自身抗体通过定制的焦点微阵列得到了验证。进一步的亚组分析显示,它与病理性近视有关,而不是单纯的没有近视性黄斑变性的高度近视。从机制上讲,抗 LIMS1 自身抗体主要属于 IgG1/IgG2/IgG3 亚类。来自病理性近视患者的血清 IgG 可通过细胞骨架紊乱和紧密连接成分减少破坏视网膜色素上皮细胞的屏障功能,还可引发视网膜色素上皮细胞中的促炎介质级联反应,而这些反应均可通过耗尽抗 LIMS1 自身抗体而减轻。总之,这些数据揭示了病理性近视中近视性黄斑变性的一种以前未被认识到的自身免疫病因。