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IL-12 unmasks latent autoimmune disease in resistant mice.

Author information

Affiliations

  • 1. Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, Maryland 20892, USA.
      Authors
    • Segal BM 1
    (1 author)

The Journal of Experimental Medicine, 01 Aug 1996, 184(2):771-775
https://doi.org/10.1084/jem.184.2.771 PMID: 8786337 PMCID: PMC2192714

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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.

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Logo of jexpmedLink to Publisher's site
J Exp Med. 1996 Aug 1; 184(2): 771–775.
PMCID: PMC2192714
PMID: 8786337

IL-12 unmasks latent autoimmune disease in resistant mice

Copyright and License information Disclaimer

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.

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Selected References

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Articles from The Journal of Experimental Medicine are provided here courtesy of The Rockefeller University Press

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