Abstract
Replying to G. J. Maghzal et al. Nature 514, 10.1038/nature13844 (2014)
After our initial observation of defective tryptophan catabolism in experimental chronic granulomatous disease (CGD)1, several laboratories have been testing the indoleamine 2,3-dioxygenase (IDO1) competence of cells from CGD patients. In most instances, they found no impairment in IDO1 competence in terms of tryptophan catabolic activity in vitro by polymorphonuclear leukocytes and monocyte-derived dendritic cells2,3, leading to the conclusion that there is no obvious defect in the production of kynurenine (the first by-product of tryptophan degradation)—hence in the IDO1-dependent mechanism of tolerogenesis as a whole in human CGD. In the accompanying Comment4, Maghzal et al. report that tryptophan catabolism is unaffected in chronic granulomatous disease, again by measurements of kynurenine production.
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Romani, L., Puccetti, P. Romani & Puccetti reply. Nature 514, E18 (2014). https://doi.org/10.1038/nature13845
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DOI: https://doi.org/10.1038/nature13845
