Cytotoxic T cell recognition of α-synuclein drives pathogenic immune responses in multiple system atrophy

J Jae-Seung Moon (Division of Immunology and Rheumatology, Department of Medicine, Stanford University) S Salvinaz I. Moutusy (Division of Immunology and Rheumatology, Department of Medicine, Stanford University) M Mengrui Zhang (Division of Immunology and Rheumatology, Department of Medicine, Stanford University) A Alain Ndayisaba (Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)) D Diego Rodriguez (Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)) D Daniel N. El Kodsi (Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)) A Anastasia Kuzkina (Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)) S Shady Younis (Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine) S Shaghayegh Jahanbani (Division of Immunology and Rheumatology, Department of Medicine, Stanford University) L Laura S. van Dam (Division of Immunology and Rheumatology, Department of Medicine, Stanford University) Y Ya’el Courtney (Division of Immunology and Rheumatology, Department of Medicine, Stanford University) A Adi Netanel (VA Palo Alto Health Care System) O Orr Sharpe (Division of Immunology and Rheumatology, Department of Medicine, Stanford University) M Mitchell G. Miglis (Department of Neurology and Neurological Sciences, Stanford University) L Lawrence Steinman (Department of Neurology and Neurological Sciences, Stanford University) V Vikram Khurana (Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)) F Fereshteh Jahanbani (Division of Immunology and Rheumatology, Department of Medicine, Stanford University) W William H. Robinson

Abstract

Multiple system atrophy (MSA) is a progressive neurologic disease, known as an α-synucleinopathy. There are currently no effective disease-modifying therapies for MSA. While neuroinflammation is a hallmark of MSA, the contribution of adaptive immune mechanisms remains poorly understood. Here, we profiled peripheral and central T cell responses in patients with MSA, in comparison with Parkinson’s disease (PD) and healthy control cohorts, using single-cell transcriptomics, flow cytometry, and antigen-specific functional assays. We demonstrated that peripheral T cells from MSA patients are activated and skewed toward cytotoxic and inflammatory phenotypes. Single-cell transcriptomics further revealed clonal expansion of cytotoxic CD8 + T cells expressing GZMB , GNLY , and chemokine and integrin programs associated with brain homing. We also demonstrated that both CD4 + and CD8 + T cells from MSA patients recognize α-synuclein monomers and preformed fibrils in an HLA class I/II-dependent manner, driving proliferation, clonal expansion, and acquisition of cytotoxic features. Consistent with these peripheral responses, CD8 + T cell density was increased in the parietal cortex of postmortem MSA brain tissues, along with cytotoxic (GZMB + , GZMK + ) and proinflammatory (IFNγ + ) CD8 + T cells. Together, these findings demonstrate that cytotoxic T cells targeting α-synuclein are engaged in MSA, suggesting that their activity may contribute to neuroinflammation and disease progression, and highlighting this immune axis as a candidate therapeutic target for further investigation.

Article Details

Volume / Issue Vol. 123, Issue 14
Published April 07, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (18)

J

Jae-Seung Moon

Division of Immunology and Rheumatology, Department of Medicine, Stanford University

S

Salvinaz I. Moutusy

Division of Immunology and Rheumatology, Department of Medicine, Stanford University

M

Mengrui Zhang

Division of Immunology and Rheumatology, Department of Medicine, Stanford University

A

Alain Ndayisaba

Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)

D

Diego Rodriguez

Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)

D

Daniel N. El Kodsi

Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)

A

Anastasia Kuzkina

Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)

S

Shady Younis

Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine

S

Shaghayegh Jahanbani

Division of Immunology and Rheumatology, Department of Medicine, Stanford University

L

Laura S. van Dam

Division of Immunology and Rheumatology, Department of Medicine, Stanford University

Y

Ya’el Courtney

Division of Immunology and Rheumatology, Department of Medicine, Stanford University

A

Adi Netanel

VA Palo Alto Health Care System

O

Orr Sharpe

Division of Immunology and Rheumatology, Department of Medicine, Stanford University

M

Mitchell G. Miglis

Department of Neurology and Neurological Sciences, Stanford University

L

Lawrence Steinman

Department of Neurology and Neurological Sciences, Stanford University

V

Vikram Khurana

Division of Movement Disorders Harvard Biomarkers Study 2.0 (HBS 2.0) and MyTrial Programs, American Parkinson Disease Association, Center for Advanced Research and MSA Center of Excellence, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s and Massachusetts General Hospitals (Mass General Brigham)

F

Fereshteh Jahanbani

Division of Immunology and Rheumatology, Department of Medicine, Stanford University

W

William H. Robinson