La Jolla Institute for Immunology and Columbia University collaborators have uncovered compelling evidence that amyotrophic lateral sclerosis (ALS) involves an autoimmune component. The study demonstrated inflammatory CD4+ T cells in patients target the C9orf72 protein, a neuronal antigen, implicating immune self-attack in ALS pathogenesis. This key insight distinguishes ALS as potentially autoimmune-driven, explaining rapid disease progression seen in many patients. The research, published in Nature, offers new therapeutic directions focusing on modulating immune responses to alter ALS outcomes and improve patient survival.