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Int J Mol Sci. 2015 Jul 21;16(7):16576-92. doi: 10.3390/ijms160716576.

B Cells and Autoantibodies in Multiple Sclerosis.

Author information

1
Department of Neurology, University Hospital Basel, Petersgraben 4 & Clinical Neuroimmunology, Hebelstrasse 20, 4031 Basel, Switzerland. anne-katrin.proebstel@usb.ch.
2
Department of Biomedicine, University of Basel, Hebelstrasse 20, 4031 Basel, Switzerland. anne-katrin.proebstel@usb.ch.
3
Department of Neurology, University Hospital Basel, Petersgraben 4 & Clinical Neuroimmunology, Hebelstrasse 20, 4031 Basel, Switzerland. nicholas.sanderson@unibas.ch.
4
Department of Biomedicine, University of Basel, Hebelstrasse 20, 4031 Basel, Switzerland. nicholas.sanderson@unibas.ch.
5
Department of Neurology, University Hospital Basel, Petersgraben 4 & Clinical Neuroimmunology, Hebelstrasse 20, 4031 Basel, Switzerland. tobias.derfuss@usb.ch.
6
Department of Biomedicine, University of Basel, Hebelstrasse 20, 4031 Basel, Switzerland. tobias.derfuss@usb.ch.

Abstract

While over the past decades T cells have been considered key players in the pathogenesis of multiple sclerosis (MS), it has only recently become evident that B cells have a major contributing role. Our understanding of the role of B cells has evolved substantially following the clinical success of B cell-targeting therapies and increasing experimental evidence for significant B cell involvement. Rather than mere antibody-producing cells, it is becoming clear that they are team players with the capacity to prime and regulate T cells, and function both as pro- and anti-inflammatory mediators. However, despite tremendous efforts, the target antigen(s) of B cells in MS have yet to be identified. The first part of this review summarizes the clinical evidence and results from animal studies pointing to the relevance of B cells in the pathogenesis of MS. The second part gives an overview of the currently known potential autoantigen targets. The third part recapitulates and critically appraises the currently available B cell-directed therapies.

KEYWORDS:

B cells; autoantibodies; autoantigen; multiple sclerosis; neuromyelitis optica; pathogenesis; therapy

PMID:
26197319
PMCID:
PMC4519967
DOI:
10.3390/ijms160716576
[Indexed for MEDLINE]
Free PMC Article

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