Romani & Puccetti reply

Replying to G. J. Maghzal et al. Nature514, 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 p...

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Bibliographic Details
Published in:Nature (London) 2014-10, Vol.514 (7523), p.E18-E18
Main Authors: Romani, L., Puccetti, P.
Format: Article
Language:English
Subjects:
631/45
Animals
brief-communications-arising
Chronic granulomatous disease
Development and progression
Diagnosis
Granulomatous Disease, Chronic - metabolism
Granulomatous Disease, Chronic - pathology
Humanities and Social Sciences
Inflammation - metabolism
Kynurenine - metabolism
Medical research
Medicine, Experimental
multidisciplinary
Science
Science (multidisciplinary)
Tryptophan - metabolism
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Summary:Replying to G. J. Maghzal et al. Nature514, 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 cells 2 , 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 Comment 4 , Maghzal et al. report that tryptophan catabolism is unaffected in chronic granulomatous disease, again by measurements of kynurenine production.
ISSN:0028-0836
1476-4687
DOI:10.1038/nature13845