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  • Title: Effects of an anti-IL-10 monoclonal antibody on rIFNbeta-1b-mediated immune modulation. Relevance to multiple sclerosis.
    Author: Porrini AM, De Luca G, Gambi D, Reder AT.
    Journal: J Neuroimmunol; 1998 Jan; 81(1-2):109-15. PubMed ID: 9521612.
    Abstract:
    The mechanism of action of recombinant IFNbeta1b (IFNbeta-1b), as a therapy for multiple sclerosis (MS), is still unknown but may result from the enhancement of ConA-induced suppressor cell function and the inhibition of IFNgamma secretion by lymphocytes. We previously demonstrated that IFNbeta-1b stimulated modest amounts of IL-10 secretion by monocytes and IL-10 activity, as cytokine synthesis inhibitory factor, was normal in MS. To determine whether IL-10 plays a role in IFNbeta-1b modulation of immune function in MS, we studied ConA-induced suppressor cell function and IFNgamma production in presence of IFNbeta-1b and an anti-IL-10 monoclonal antibody (mAb). Anti-IL-10 mAb significantly reduced the effect of IFNbeta-1b on ConA-induced suppressor cell function and IFNgamma production in healthy subjects; MS patients showed a trend of inhibition. We hypothesized that IL-10 may play a role in mediating the effects of IFNbeta-1b on suppressor cell function and IFNgamma production but suppressor molecules other than IL-10 could be also involved.
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