Ingested (oral) rituximab inhibits EAE

- MAb against CD20, rituximab (RTX) (Rituxan®), was used in EAE by the oral route.
- Oral RTX inhibited ongoing disease and decreased inflammation in actively fed mice and adoptively treated recipients.
- Transferred cells from RTX fed donors protected against EAE.
- RTX decreased TNF-α, IL-12, IFN-γ, IL-17 (Teff) in active fed mice and adoptively treated recipients.
- RTX did not increased Th2-like cytokine IL-4, IL-10, IL-13 in active fed mice and adoptively treated recipients.

BackgroundBlocking CD20 can inhibit autoimmune diseases such as multiple sclerosis (MS) and rheumatoid arthritis (RA).ObjectiveWe examined whether an antibody against CD20, rituximab (RTX) (Rituxan®), used clinically in oncology, MS and RA would have similar anti-inflammatory effects in EAE after oral administration.Design/methodsB6 mice were immunized with MOG peptide 35-55 and gavaged with control saline or RTX during ongoing disease. Splenocytes or CD4+ T cells from control fed or RTX fed mice were adoptively transferred into active MOG peptide 35-55 immunized recipient mice during ongoing disease. Actively fed and recipient mice were examined for disease inhibition, inflammation, and cytokine responses.ResultsIngested (oral) RTX inhibited ongoing disease and decreased inflammation. Adoptively transferred cells from RTX fed donors protected against actively induced disease and decreased inflammation. There was a decrease in Th1-like cytokines IFN-γ and IL-12, IL-17 and TNF-α in active fed and adoptively treated recipients without upregulation of counter-regulatory cytokines.ConclusionsIngested (orally administered) RTX can inhibit disease, CNS inflammation, decrease pro-inflammatory IL-17 and Th1-like cytokines without increases in Th2-like anti-inflammatory cytokines.