Rituximab treatment reduces organ-specific T cell effector responses and ameliorates Experimental Autoimmune Encephalomyelitis (107.3)

TL;DRAbstract

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). However, 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. EAE severity was reduced in a therapeutic model and EAE symptoms were not observed in a preventive model. 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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