免疫系统
生物
肌萎缩侧索硬化
神经炎症
C9orf72
神经科学
重编程
先天免疫系统
转录组
脊髓
小胶质细胞
炎症
补体系统
多发性硬化
免疫学
获得性免疫系统
髓样
单核细胞
神经退行性变
中枢神经系统
神经免疫学
主要组织相容性复合体
作者
Ziyang Zhang,Lynn van Olst,Francesco Alessandrini,Matthew Wright,Alex J. Edwards,Jake Sondag Boles,Anait Nalbandian,Anne V. Forsyth,Nate Shepard,Thomas H. Watson,Evan Kaspi,Angeli Mittal,Joshua Kuruvilla,Natalie Piehl,Abhirami Ramakrishnan,Stanley H. Appel,Evangelos Kiskinis,David Gate
标识
DOI:10.1038/s41593-026-02300-5
摘要
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder marked by progressive motor neuron (MN) degeneration in the brain and spinal cord. Although neuroinflammation is increasingly recognized as a hallmark of ALS, the precise molecular programs linking immune responses to MN pathology remain poorly defined. Using an integrated approach that combines single-cell and bulk RNA sequencing with spatial proteogenomics, we characterized both shared and distinct immune dynamics in peripheral blood and spinal cord tissues from patients with sporadic ALS and those carrying C9orf72 repeat expansions. Our analysis revealed broad immune remodeling in C9orf72 ALS, ALS subtype-specific and progression-associated differences in monocyte activation and antigen-experienced CD8 effector memory T cells with clonal features consistent with antigen-driven responses. Spatial mapping revealed complement activation and lipid-programmed myeloid states converging at sites of MN loss and TDP-43 pathology. Together, these findings connect peripheral and central immune alterations to ALS heterogeneity and highlight stratified immunomodulation as a potential therapeutic strategy.
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