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Effect of indoleamine 2,3-dioxygenase on induction of experimental autoimmune encephalomyelitis

  1. Author:
    Sakurai, K.
    Zou, J. P.
    Tschetter, J. R.
    Ward, J. M.
    Shearer, G. M.

  2. Author Address

    NCI, Expt Immunol Branch, NIH, Bldg 10,Room 4B36,9000 Rockville Pike, Bethesda, MD 20892 USA NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA NCI, NIH, Frederick, MD 21702 USA Shearer GM NCI, Expt Immunol Branch, NIH, Bldg 10,Room 4B36,9000 Rockville Pike, Bethesda, MD 20892 USA
    1. Year: 2002
  2. Journal: Journal of Neuroimmunology
    1. 129
    2. 1-2
    3. Pages: 186-196
  4. Type of Article: Article
  1. Abstract:

    Experimental autoimmune encephalomyelitis (EAE) is a T cell- mediated demyelinating disease of the central nervous system (CNS). Indoleamine 2,3-dioxygenase (IDO) is an enzyme that catabolizes tryptophan, which can result in the death of T lymphocytes. This effect of IDO is inhibited by 1-methyl- tryptophan (1-MT). We used a murine model of EAE to demonstrate; (1) opposing patterns of spinal cord IDO and interferon-gamma (INF-gamma) mRNA expression through the preclinical, acute and remission I phases of EAE; (2) a change in the kynurenine-to-tryptophan (KIT) ratio during these same phases; and (3) 1-MT-induced exacerbation of clinical and histologic disease parameters during EAE. These results suggest that IDO may contribute to the regulation of T cell activity associated with the different phases of this animal model of multiple sclerosis (MS). (C) 2002 Elsevier Science B.V. All rights reserved.

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