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Impaired macrophage function following bacterial stimulation in chronic granulomatous disease
Author(s) -
Rahman Farooq Z.,
Hayee Bu’Hussain,
Chee Ronnie,
Segal Anthony W.,
Smith Andrew M.
Publication year - 2009
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2009.03112.x
Subject(s) - chronic granulomatous disease , nadph oxidase , nicotinamide adenine dinucleotide phosphate , biology , immunology , phagocyte , macrophage , innate immune system , immunity , acquired immune system , oxidase test , primary immunodeficiency , microbiology and biotechnology , immune system , reactive oxygen species , enzyme , biochemistry , in vitro
Summary Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is critical for phagocyte anti‐microbial activity and plays a major role in innate immunity. Defects in genes coding for components of the NADPH oxidase enzyme system are responsible for chronic granulomatous disease (CGD), a rare primary neutrophil immunodeficiency associated with recurrent, life‐threatening bacterial and fungal infections. Microbial killing and digestion within the neutrophil phagosomal compartment are defective in these patients. NADPH oxidase activity is also crucial for optimal macrophage and dendritic cell function and has recently been implicated in both cross‐presentation and T‐cell priming. We present evidence of impaired macrophage function in CGD, with attenuated pro‐inflammatory cytokine and increased interleukin‐10 secretion following bacterial stimulation. These results highlight additional abnormalities in macrophage function associated with CGD and the importance of NADPH oxidase activity in immunity.