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

Nancy L. Monson, Petra Cravens, Rehana Hussain, Christopher T. Harp, Matthew Cummings, Maria de Pilar Martin, Li Hong Ben, Julie Do, Jeri Anne Lyons, Amy Lovette-Racke, Anne H. Cross, Michael K. Racke, Olaf Stüve, Mark Shlomchik, Todd N. Eagar

Research output: Contribution to journalArticlepeer-review

70 Scopus citations

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.

Original languageEnglish
Article numbere17103
JournalPloS one
Volume6
Issue number2
DOIs
StatePublished - 2011

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