Prevention of experimental allergic encephalomyelitis via inhibition of IL-12 signaling and IL-12-mediated Th1 differentiation: an effect of the novel anti-inflammatory drug lisofylline

J Immunol. 1998 Dec 15;161(12):7015-22.

Abstract

Experimental allergic encephalomyelitis (EAE) is an inflammatory, CD4+ Th1-mediated autoimmune disease, which serves as a model for multiple sclerosis. We examined the effect of a novel anti-inflammatory drug, lisofylline (LSF), on EAE induced either by injection of mouse spinal cord homogenate or following transfer of myelin basic protein-reactive T cells. Orally administered LSF significantly inhibited EAE in both cases, decreasing peak clinical scores by >70% and >80%, respectively. In addition, analysis of representative spinal cord sections from LSF-treated mice showed complete lack of demyelination and lymphocyte infiltration. The reduction in EAE correlated with the inhibition of Th1 differentiation by LSF in vivo, as indicated by a reduction in T cell IFN-gamma production ex vivo after Ag restimulation. The inhibition of Th1 differentiation in vivo is consistent with a block in IL-12 receptor signaling, because LSF blocked IL-12-driven Th1 differentiation and T cell proliferation in vitro, yet had no effect on IL-12 secretion from APCs ex vivo or in vitro.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adoptive Transfer
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
  • Autoimmune Diseases / drug therapy
  • Autoimmune Diseases / immunology
  • Autoimmune Diseases / prevention & control*
  • Cell Differentiation / drug effects
  • Drug Evaluation, Preclinical
  • Encephalomyelitis, Autoimmune, Experimental / drug therapy
  • Encephalomyelitis, Autoimmune, Experimental / immunology
  • Encephalomyelitis, Autoimmune, Experimental / prevention & control*
  • Female
  • Gene Expression Regulation / drug effects
  • Immunization
  • Interferon-gamma / biosynthesis
  • Interferon-gamma / genetics
  • Interleukin-12 / antagonists & inhibitors
  • Interleukin-12 / metabolism
  • Interleukin-12 / physiology*
  • Interleukin-4 / biosynthesis
  • Interleukin-4 / genetics
  • Lymphocyte Activation / drug effects
  • Mice
  • Mice, Inbred Strains
  • Myelin Basic Protein / immunology
  • Pentoxifylline / analogs & derivatives*
  • Pentoxifylline / pharmacology
  • Pentoxifylline / therapeutic use
  • Recombinant Proteins / pharmacology
  • Severity of Illness Index
  • Signal Transduction / drug effects*
  • Th1 Cells / cytology
  • Th1 Cells / drug effects*
  • Th1 Cells / immunology
  • Th1 Cells / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Myelin Basic Protein
  • Recombinant Proteins
  • Interleukin-12
  • Interleukin-4
  • Interferon-gamma
  • lisofylline
  • Pentoxifylline