IL-12 unmasks latent autoimmune disease in resistant mice

J Exp Med. 1996 Aug 1;184(2):771-5. doi: 10.1084/jem.184.2.771.

Abstract

Inbred mice exhibit a spectrum of susceptibility to induction of experimental allergic encephalomyelitis (EAE). We have compared the immune responses of the susceptible SJL (H-2s) and resistant B10.S (H-2s) strains to determine factors other than the MHC background which control resistance/susceptibility to EAE. The resistance of the B10.S strain was found to be secondary to an antigen-specific defect in the generation of Th 1 cells that produce IFN gamma. This defect in IFN gamma production could be restored by exposure of the myelin basic protein (MBP)-reactive T cells to IL-12 with the subsequent induction of the ability to transfer EAE to naive recipients. These findings have important implications for the therapeutic use of IL-12 and IL-12 antagonists and may explain the association between relapses/exacerbation of autoimmune disease and infectious diseases.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Female
  • Interferon-gamma / biosynthesis
  • Interleukin-12 / immunology*
  • Mice
  • Mice, Inbred Strains
  • Mice, Mutant Strains
  • Molecular Sequence Data
  • Myelin Basic Protein / chemistry
  • Myelin Basic Protein / immunology*
  • Th1 Cells / immunology

Substances

  • Myelin Basic Protein
  • Interleukin-12
  • Interferon-gamma