Authors
Martin S Weber, Thomas Prod'Homme, Juan C Patarroyo, Nicolas Molnarfi, Tara Karnezis, Klaus Lehmann‐Horn, Dimitry M Danilenko, Jeffrey Eastham‐Anderson, Anthony J Slavin, Christopher Linington, Claude CA Bernard, Flavius Martin, Scott S Zamvil
Publication date
2010/9
Journal
Annals of neurology
Volume
68
Issue
3
Pages
369-383
Publisher
Wiley Subscription Services, Inc., A Wiley Company
Description
Objective
Clinical studies indicate that anti‐CD20 B‐cell depletion may be an effective multiple sclerosis (MS) therapy. We investigated mechanisms of anti‐CD20‐mediated immune modulation using 2 paradigms of experimental autoimmune encephalomyelitis (EAE).
Methods
Murine EAE was induced by recombinant myelin oligodendrocyte glycoprotein (rMOG), a model in which B cells are considered to contribute pathogenically, or MOG peptide (p)35‐55, which does not require B cells.
Results
In EAE induced by rMOG, B cells became activated and, when serving as antigen‐presenting cells (APCs), promoted differentiation of proinflammatory MOG‐specific Th1 and Th17 cells. B‐cell depletion prevented or reversed established rMOG‐induced EAE, which was associated with less central nervous system (CNS) inflammation, elimination of meningeal B cells, and reduction of MOG‐specific Th1 and Th17 cells …
Total citations
Scholar articles
MS Weber, T Prod'Homme, JC Patarroyo, N Molnarfi… - Annals of neurology, 2010