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Author Spotlight: Novel Assay for Studying B-Cell Responses in Multiple Sclerosis Research
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A pathogenic and clonally expanded B cell transcriptome in active multiple sclerosis.

Akshaya Ramesh1,2, Ryan D Schubert1,2, Ariele L Greenfield1,2

  • 1Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.

Proceedings of the National Academy of Sciences of the United States of America
|August 30, 2020
PubMed
Summary
This summary is machine-generated.

In multiple sclerosis (MS), B cells in the cerebrospinal fluid (CSF) show inflammatory and expanded phenotypes. These CSF B cells are linked to disease activity and intrathecal immunoglobulin synthesis, not viral infections.

Keywords:
B cellimmune repertoiremultiple sclerosisneuroimmunology

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Area of Science:

  • Neuroimmunology
  • Cellular immunology
  • Molecular biology

Background:

  • B cells in the central nervous system (CNS) play multifaceted roles in multiple sclerosis (MS), including cytokine secretion, antigen presentation, antibody production, and potential viral reservoirs.
  • Understanding the specific functions and phenotypes of B cells within the CNS is crucial for elucidating MS pathogenesis.

Purpose of the Study:

  • To investigate the roles and phenotypes of B cells in the cerebrospinal fluid (CSF) of individuals with relapsing-remitting MS (RRMS) compared to other neurologic diseases (ONDs) and healthy controls (HCs).
  • To identify molecular pathways and cellular characteristics of CSF B cells associated with MS activity.

Main Methods:

  • Single-cell RNA sequencing (scRNA-Seq) and single-cell immunoglobulin sequencing (scIg-Seq) were performed on paired CSF and blood samples.
  • Bulk RNA sequencing (RNA-Seq) was conducted on isolated CSF and blood B cell subsets.
  • Analysis included pathway activation, receptor up-regulation, and clonal expansion of B cells.

Main Results:

  • Activated nuclear factor kappa B (NF-κB) and cholesterol biosynthesis pathways were observed in CSF memory B cells.
  • Down-regulated SMAD/TGF-β1 signaling was noted in CSF plasmablasts/plasma cells.
  • Clonally expanded, somatically hypermutated IgM+ and IgG1+ CSF B cells correlated with inflammation, blood-brain barrier breakdown, and intrathecal immunoglobulin synthesis. No viral transcripts were detected.

Conclusions:

  • CSF B cells in MS exhibit an inflammatory and clonally expanded memory and plasmablast/plasma cell phenotype.
  • These findings support the role of CNS B cells in driving MS pathogenesis through inflammatory mechanisms rather than viral triggers.