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Related Experiment Video

Updated: Jan 13, 2026

Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
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B cell tolerance checkpoint function in multiple sclerosis and transient CD52 depletion.

Anastasia Alexaki1, Fotis Baltoumas2, Dimitrios Tzanetakos3

  • 1First Department of Neurology, National and Kapodistrian University of Athens, Greece.

Journal of Neuroimmunology
|January 8, 2026
PubMed
Summary
This summary is machine-generated.

Alemtuzumab treatment for multiple sclerosis did not alter B cell tolerance checkpoints. Secondary autoimmunity risk was not linked to B cell autoreactivity after alemtuzumab (anti-CD52) therapy.

Keywords:
AlemtuzumabB cell toleranceCD52Multiple sclerosis

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Area of Science:

  • Immunology
  • Neuroimmunology
  • Autoimmunity

Background:

  • Alemtuzumab (anti-CD52) effectively treats relapsing-remitting multiple sclerosis (MS).
  • Alemtuzumab can cause secondary autoimmunity, but its effect on B cell tolerance is unknown.
  • Understanding B cell tolerance is crucial for managing MS and its treatments.

Purpose of the Study:

  • To evaluate peripheral B cell tolerance checkpoint integrity in alemtuzumab-treated MS patients.
  • To investigate the relationship between B cell autoreactivity and secondary autoimmunity post-alemtuzumab.
  • To analyze B cell receptor (BCR) repertoire parameters in relation to tolerance mechanisms.

Main Methods:

  • Constructed 138 recombinant monoclonal antibodies (mAbs) from single mature naïve B cells.
  • Tested mAbs for poly- and autoreactivity in healthy donors (HDs), immunotherapy-naïve MS patients, and alemtuzumab-treated MS patients.
  • Analyzed B cell receptor (BCR) repertoire parameters, including complementarity-determining region 3 (CDR3) net charge.

Main Results:

  • No significant differences in polyreactive and autoreactive B cell fractions were found among the groups.
  • Autoreactive B cell fractions did not correlate with secondary autoimmunity or future MS activity.
  • Alemtuzumab-treated patients showed a lower mean naïve CDR3 net charge compared to HDs, an isolated finding.

Conclusions:

  • Transient CD52 depletion with alemtuzumab does not appear to significantly alter peripheral B cell tolerance checkpoints.
  • Secondary autoimmunity risk is unlikely to be directly linked to major changes in B cell autoreactivity post-treatment.
  • Findings may inform other immune reconstitution therapies in MS and related conditions.