Abstract
Regulation of immune responses through local catabolic depletion of tryptophan (Trp) was first identified in studies of the maternal T cell response to the fetus. This pathway, which is controlled by the enzyme indoleamine 2,3-dioxygenase (IDO), has since been identified in a variety of immunological settings. Platten et al. now find that IDO-mediated Trp catabolism also contributes during therapy of a mouse model of multiple sclerosis. By using a form of antigen termed an altered peptide ligand, T cell responses were prevented from causing inflammation and nervous system pathology, and this effect corresponded with the induction of IDO. Naturally occurring metabolites and a synthetic derivative of the IDO pathway inhibited T cell proliferation and activation of antigen-presenting cells. Remarkably, paralyzed mice recovered after being fed the synthetic derivative. M. Platten, P. P. Ho, S. Youssef, P. Fontoura, H. Garren, E. M. Hur, R. Gupta, L. Y. Lee, B. A. Kidd, W. H. Robinson, R. A. Sobel, M. L. Selley, L. Steinman, Treatment of autoimmune neuroinflammation with a synthetic tryptophan metabolite. Science 310 , 850-855 (2005). [Abstract] [Full Text]
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