IL-10 fails to abrogate experimental autoimmune encephalomyelitis

B. Cannella, Y. L. Gao, C. Brosnan, C. S. Raine

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Mice adoptively-sensitized to develop chronic relapsing experimental autoimmune encephalomyelitis (EAE), a model for the human demyelinating condition, multiple sclerosis (MS), were given injections of recombinant human IL-10 at various timepoints postsensitization in an attempt to abrogate disease development. IL-10 is a Th2 immunomodulatory cytokine with known down-regulatory effects upon Th1 responses and macrophages. Contrary to a previous report on EAE and the predicted outcome, after repeated experiments, IL-10 was found to elicit a worsening or no effect upon EAE in the mouse. Animals were studied clinically, histopathologically and immunocytochemically. On no occasion was disease ameliorated by IL-10. Pretreatment with IL-10 of lymph node cells used to transfer EAE had no effect upon disease outcome, indicating that the cells were already committed effectors. Administration of anti-IL-10 monoclonal antibody before onset of signs had no effect when given early post-sensitization and caused marked worsening when given immediately before onset of signs. In the context of this autoimmune demyelinating model, these results suggest that IL-10 alone is insufficient to reverse the effector response and indeed may serve to enhance the cascade of events in EAE.

Original languageEnglish (US)
Pages (from-to)735-746
Number of pages12
JournalJournal of Neuroscience Research
Issue number6
StatePublished - Sep 15 1996


  • autoimmunity
  • cytokines
  • multiple sclerosis
  • myelin
  • neuropathology

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


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