Rituximab, the monoclonal antibody against B lymphocyte protein CD20, is a major asset for treatment of diseases in which B CD20 cells are the foremost etiologic culprit. Based on observations that rituximab is capable to modulate immune responses the question if the drug may affect the capacity of human peripheral blood mononuclear cells (PBMC) for cytokine production was posed.
PBMC were incubated without or with various concentrations of rituximab and the production of TNFα, IL-1β, IL-6, IFNγ, IL-2, IL-1ra and IL-10 was examined using the ELISA method.
While rituximab did not impel non-stimulated PBMC to produce any of the cytokines examined, cells stimulated with PMA/ionomycin expressed a concentration-dependent inhibition of the pro-inflammatory cytokines IL-2 and IFNγ. Following LPS stimulation the secretion of TNFα was slightly increased. Notably, the production of the anti-inflammatory cytokine IL-10 was restrained, but at lesser extend in comparison to the effect of rituximab on the pro-inflammatory cytokine secretion.
The results indicate that rituximab in addition to its efficacy as an antibody against CD20 receptor expressing cells, 'exerts immunomodulatory activity by targeting their capacity for inflammatory cytokine production.