IL-10 FAILS TO ABROGATE EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS

Mice adoptively-sensitized to develop chronic relapsing experimental a utoimmune encephalomyelitis (EAE), a model for the human demyelinating condition, multiple sclerosis (MS), were given injections of recombin ant human IL-10 at various timepoints post-sensitization in an attempt to abrogate disease development, IL-10 is a Th2 immunomodulatory cyto kine with known down-regulatory effects upon Th1 responses and macroph ages, Contrary to a previous report on EAE and the predicted outcome, after repeated experiments, IL-10 was found to elicit a worsening or n o effect upon EAE in the mouse, Animals were studied clinically, histo pathologically and immunocytochemically, On no occasion was disease am eliorated by IL-10. Pretreatment with IL-10 of lymph node cells used t o transfer EAE had no effect upon disease outcome, indicating that the cells were already committed effecters, Administration of anti-IL-10 monoclonal antibody before onset of signs had no effect when given ear ly post-sensitization and caused marked worsening when given immediate ly before onset of signs, In the context of this autoimmune demyelinat ing model, these results suggest that IL-10 alone is insufficient to r everse the effector response and indeed may serve to enhance the casca de of events in EAE. (C) 1996 Wiley-Liss, Inc.