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We hypothesized that B lymphocytes are involved in Parkinson\u2019s disease progression. We measured antibodies to alpha-synuclein and tau in serum from patients with rapid eye movement sleep behaviour disorder (n = 79), early Parkinson\u2019s disease (n = 50) and matched controls (n = 50). Rapid eye movement sleep behaviour disorder cases were stratified by risk of progression to Parkinson\u2019s disease (low risk = 30, high risk = 49). We also measured B-cell activating factor of the tumour necrosis factor receptor family, C-reactive protein and total immunoglobulin G. We found elevated levels of antibodies to alpha-synuclein fibrils in rapid eye movement sleep behaviour disorder patients at high risk of Parkinson\u2019s disease conversion (ANOVA, P &amp;lt; 0.001) and lower S129D peptide-specific antibodies in those at low risk (ANOVA, P &amp;lt; 0.001). An early humoral response to alpha-synuclein is therefore detectable prior to the development of Parkinson\u2019s disease. Peripheral B lymphocyte phenotyping using flow cytometry in early Parkinson\u2019s disease patients and matched controls (n = 41 per group) revealed reduced B cells in Parkinson\u2019s disease, particularly in those at higher risk of developing an early dementia [t(3) = 2.87, P = 0.01]. Patients with a greater proportion of regulatory B cells had better motor scores [F(4,24) = 3.612, P = 0.019], suggesting they have a protective role in Parkinson\u2019s disease. In contrast, B cells isolated from Parkinson\u2019s disease patients at higher risk of dementia had greater cytokine (interleukin 6 and interleukin 10) responses following in vitro stimulation. We assessed peripheral blood lymphocytes in alpha-synuclein transgenic mouse models of Parkinson\u2019s disease: they also had reduced B cells, suggesting this is related to alpha-synuclein pathology. In a toxin-based mouse model of Parkinson\u2019s disease, B-cell deficiency or depletion resulted in worse pathological and behavioural outcomes, supporting the conclusion that B cells play an early protective role in dopaminergic cell loss. In conclusion, we found changes in the B-cell compartment associated with risk of disease progression in rapid eye movement sleep behaviour disorder (higher alpha-synuclein antibodies) and early Parkinson\u2019s disease (lower levels of B lymphocytes that were more reactive to stimulation). Regulatory B cells play a protective role in a mouse model, potentially by attenuating inflammation and dopaminergic cell loss. B cells are therefore likely to be involved in the pathogenesis of Parkinson\u2019s disease, albeit in a complex way, and thus warrant consideration as a therapeutic target.<\/jats:p>","DOI":"10.1093\/braincomms\/fcad060","type":"journal-article","created":{"date-parts":[[2023,3,9]],"date-time":"2023-03-09T10:47:23Z","timestamp":1678358843000},"source":"Crossref","is-referenced-by-count":52,"title":["B lymphocyte responses in Parkinson\u2019s disease and their possible significance in disease progression"],"prefix":"10.1093","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3121-5963","authenticated-orcid":false,"given":"Kirsten M","family":"Scott","sequence":"first","affiliation":[{"name":"John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge , Cambridge CB2 0PY , UK"},{"name":"Molecular Immunity Unit, Department of Medicine, University of Cambridge , Cambridge CB2 0QH , 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