Interleukin-10 prevents experimental allergic encephalomyelitis in rats

Eur J Immunol. 1994 Jun;24(6):1434-40. doi: 10.1002/eji.1830240629.


Experimental allergic encephalomyelitis (EAE) is an autoimmune disease mediated by myelin protein-specific CD4+ T lymphocytes of the T(h)1-like phenotype. In rats, the disease is characterized by a monophasic clinical manifestation, followed by a subsequent spontaneous remission and the establishment of life-long resistance to reinduction of disease. Recent data indicate that intracerebral cytokine production, in particular synthesis of interleukin(IL)-10, is selectively up-regulated during the recovery phase of disease. This led us to assess the effects of IL-10 on different rat lymphoid cell functions in vitro and to consider the possibility of an IL-10-mediated treatment to prevent the induction of central nervous system (CNS) autoimmune disease in vivo. Human recombinant IL-10 suppressed interferon-gamma induced major histocompatibility complex class II up-regulation in rat peritoneal macrophages, exhibited pleiotropic effects on thymocytes and totally abrogated tumor necrosis factor production of encephalitogenic T lymphocytes in vitro, without simultaneously affecting proliferative responses of the cells. Upon systemic administration during the initiation phase of disease, IL-10 was effective in markedly suppressing the subsequent induction of EAE in Lewis rats. This suppression of clinical disease coincided with a significant and specific elevation of myelin basic protein-specific autoantibody production, a sustained T cell proliferative response to myelin basic protein and a diminution of CNS infiltrations and thymic involutions in diseased animals. These data implicate IL-10 as a possible candidate for treatment of T(h)1-mediated CNS (auto-) immune diseases.

MeSH terms

  • Animals
  • Cells, Cultured
  • Encephalomyelitis, Autoimmune, Experimental / immunology
  • Encephalomyelitis, Autoimmune, Experimental / prevention & control*
  • Flow Cytometry
  • Histocompatibility Antigens Class II / biosynthesis
  • Interleukin-10 / therapeutic use*
  • Lymphocyte Activation
  • Macrophages / drug effects
  • Myelin Basic Protein / immunology
  • Rats
  • Rats, Inbred Lew
  • T-Lymphocyte Subsets / drug effects
  • Thymus Gland / cytology
  • Thymus Gland / drug effects
  • Tumor Necrosis Factor-alpha / biosynthesis


  • Histocompatibility Antigens Class II
  • Myelin Basic Protein
  • Tumor Necrosis Factor-alpha
  • Interleukin-10