Comprehensive cerebrospinal fluid analysis indicates key roles for B cells in multiple sclerosis

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Item Type:	Preprint
Title:	Comprehensive cerebrospinal fluid analysis indicates key roles for B cells in multiple sclerosis
Creators Name:	Fernández-Zapata, C., Otto, C., Gallaccio, G., Chen, Q., Wang, M., Uluvar, B., Teves, M., Samol, C., Buthut, M., Bösl, F.R., Dehlinger, A., Jang, G.H., Böttcher, C., Radbruch, H., Priller, J., Schindler, P., Raposo, C., Shippling, S., Pedotti, R., Kunkel, D., Pietzner, M., Franke, C., Oefner, P.J., Gronwald, W., Prüß, H., Lohmeier, J., Paul, F., Ruprecht, K. and Böttcher, C.
Abstract:	Multiple sclerosis (MS) is a complex inflammatory and neurodegenerative disease of the central nervous system (CNS) with a multifaceted pathophysiology, likely involving a variety of mechanisms and effectors. To characterize the spectrum of cellular and molecular factors involved in MS at an unprecedented level, we here performed a comprehensive analysis of cerebrospinal fluid (CSF) and peripheral blood using multiple high-dimensional technologies, including mass cytometry, metabolomics and proteomics (NULISA and Olink Explore® 3072). Enriched B cells and proteins involved in B cell functions in the CSF separated MS patients from other neurological disease entities. Specific B cell subpopulations and molecular markers including gut-microbiota-derived metabolites and neurofilament light protein, a marker of neuroaxonal damage, in CSF correlated with clinical (acute vs. stable disease) and/or radiological (gadolinium enhancement) disease activity. Altogether, unbiased broad phenotyping suggests key roles of diverse B subpopulations and B cell related molecular markers in MS, which are associated with both, inflammatory and degenerative aspects of the disease and may serve as disease activity and treatment response biomarkers.
Source:	medRxiv
Publisher:	Cold Spring Harbor Laboratory Press
Article Number:	2025.01.02.24319302
Date:	6 January 2025
Official Publication:	https://doi.org/10.1101/2025.01.02.24319302

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