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Research Anti-CD20 B-cell depletion enhances monocyte reactivity in neuroimmunological disorders Klaus Lehmann-Horn , Eva Schleich , Deetje Hertzenberg , Alexander Hapfelmeier , Tania Kuempfel , Nikolas von Bubnoff , Reinhard Hohlfeld , Achim Berthele , Bernhard Hemmer and Martin S Weber ? For all author emails, please log on . Journal of Neuroinflammation 2011, 8 :146? doi:10.1186/1742-2094-8-146 Published: 26 October 2011 Abstract (provisional) Background Clinical trials evaluating anti-CD20-mediated B-cell depletion in multiple sclerosis (MS) and neuromyelitis optica (NMO) generated encouraging results.
Aquaporin-4 (AQP4) deficiency in mice reduces neuroinflammation in experimental autoimmune encephalomyelitis (EAE) produced by active immunization with myelin oligodendrocyte glycoprotein peptide (MOG).
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.