Rituximab therapy reduces organ-specific T cell responses and ameliorates experimental autoimmune encephalomyelitis

Monson NL, Cravens P, Hussain R, Harp CT, Cummings M, de Pilar Martin M, Ben LH, Do J, Lyons JA, Lovette-Racke A, Cross AH, Racke MK, Stüve O, Shlomchik M, Eagar TN (2011). PLoS One, 6(2):e17103
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Abstract

Recent clinical trials have established B cell depletion by the anti-CD20 chimeric antibody Rituximab as a beneficial therapy for patients with relapsing-remitting multiple sclerosis (MS). The impact of Rituximab on T cell responses remains largely unexplored. In the experimental autoimmune encephalomyelitis (EAE) model of MS in mice that express human CD20, Rituximab administration rapidly depleted peripheral B cells and strongly reduced EAE severity. B cell depletion was also associated with diminished Delayed Type Hypersensitivity (DTH) and a reduction in T cell proliferation and IL-17 production during recall immune response experiments. While Rituximab is not considered a broad immunosuppressant, our results indicate a role for B cells as a therapeutic cellular target in regulating encephalitogenic T cell responses in specific tissues.

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Posted on October 14, 2011
Posted in: Axon Injury & Repair, Publications Authors: