Journal of Neuroimmunology, Vol. 129 (1-2) (2002) pp. 186-196
Kenichi Sakurai a, Jian-Ping Zou a, Jolynne R. Tschetter a, Jerrold M. Ward b and Gene M. Shearer a
a Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Building 10, Room 4B36, 9000 Rockville Pike, Bethesda, MD 20892, USA
b Veterinary Pathology, National Cancer Institute, National Institutes of Health, Frederick, MD 21702-1201, USA
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- (INF-) mRNA expression through the preclinical, acute and remission I phases of EAE; (2) a change in the kynurenine-to-tryptophan (K/T) 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).
© 2002 Elsevier Science B.V.