Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6063382 | Journal of Allergy and Clinical Immunology | 2015 | 23 Pages |
Abstract
Together, the data support the hypothesis that signaling from the NADPH oxidase under normal circumstances governs phagocyte mtROS production and that such signaling is lacking in the absence of a functioning phagocyte oxidase. PPARγ agonism appears to bypass the need for the NADPH oxidase for enhanced mtROS production and partially restores host defense in CGD.
Keywords
DPICFUphorbol 12-myristate 13-acetatemtROSCGDDHRPPARNADPHPMAROSOxidantsBADGEchronic granulomatous diseasedihydrorhodaminediphenylene iodoniumSODSuperoxide dismutasePhagocytesMitochondriawild-typeNAD, nicotinamide adenine dinucleotidecolony-forming unitsmitochondrial reactive oxygen speciesReactive oxygen speciesPeroxisome proliferator–activated receptor
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Authors
Ruby F. PhD, S. Courtney PhD, Stacey M. MS, Kenneth C. PhD, Michael PhD, Ronald J. PhD, Claudia V. PhD, Raphael PhD, Peter M. MD, PhD, Steven M. MD, Donna L. MD,