The DOI matches its Crossref record; 121 of the 121 references it cites were found in a registry or an index.
Role of Nox Family NADPH Oxidases in Host Defense
Abstract
The phagocytic NADPH oxidase is recognized as a critical component of innate immunity, responsible for generation of microbicidal reactive oxygen species (ROS). This enzyme is one representative of the Nox family of oxidases (Nox1-Nox5, Duox1, and Duox2) that exhibit diverse expression patterns and appear to serve a variety of functions related to ROS generation. Mounting evidence now suggests that several of these novel oxidases also serve in host defense, particularly those showing high expression along epithelial surfaces exposed to the external environment. Within these sites, Nox enzymes tend to be located on apical cell surfaces and release ROS into extracellular environments, where they can be used by known antimicrobial peroxidases. Moreover, microbial factors were shown in several cases to cause higher ROS production, either by direct oxidase activation or by inducing higher oxidase expression. Several oxidases are also induced by immune cytokines, including interferon-gamma, interleukin (IL)-4, and IL-13. Although most of the evidence supporting host defense roles for mammalian nonphagocytic oxidases remains circumstantial, recent evidence indicates that Drosophila Duox plays a role in host resistance to infection. Finally, oxidative defense against invading pathogens appears to be an ancient protective mechanism, because related oxidases are known to participate in disease resistance in plants.
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Citations
Cites
1 retracted
The large-conductance Ca2+-activated K+ channel is essential for innate immunity
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RetractedSystematic functional analysis of the Caenorhabditis elegans genome using RNAi
Kamath, R. S., Fraser, A. G., Dong, Y., Poulin, G., Durbin, R., Gotta, M., Kanapin, A., Le Bot, N., Moreno, S., Sohrmann, M., et al. (2003) · Nature · doi:10.1038/nature01278 · Cited by 3,616
THE OXIDATIVE BURST IN PLANT DISEASE RESISTANCE
Lamb, C., & Dixon, R. A. (1997) · Annual Review of Plant Physiology and Plant Molecular Biology · doi:10.1146/annurev.arplant.48.1.251 · Cited by 3,213
NOX enzymes and the biology of reactive oxygen
Lambeth, J. D. (2004) · Nature Reviews Immunology · doi:10.1038/nri1312 · Cited by 3,125
Interleukin-13: Central Mediator of Allergic Asthma
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The immunological and genetic basis of inflammatory bowel disease
Bouma, G., & Strober, W. (2003) · Nature Reviews Immunology · doi:10.1038/nri1132 · Cited by 1,767
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Cited by
Ying, W. (2008) · Antioxidants & Redox Signaling · doi:10.1089/ars.2007.1672 · Cited by 1,494
Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets
Drummond, G. R., Selemidis, S., Griendling, K. K., & Sobey, C. G. (2011) · Nature Reviews Drug Discovery · doi:10.1038/nrd3403 · Cited by 899
Nox proteins in signal transduction
Brown, D. I., & Griendling, K. K. (2009) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2009.07.023 · Cited by 832
NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology
Vermot, A., Petit-Härtlein, I., Smith, S. M. E., & Fieschi, F. (2021) · Antioxidants · doi:10.3390/antiox10060890 · Cited by 766
T cell lipid peroxidation induces ferroptosis and prevents immunity to infection
Matsushita, M., Freigang, S., Schneider, C., Conrad, M., Bornkamm, G. W., & Kopf, M. (2015) · Journal of Experimental Medicine · doi:10.1084/jem.20140857 · Cited by 672
“Although it has become widely understood that T cells can in fact up-regulate xc upon activation, T cells in the early stages of activation still require cysteine from other sources (Levring et al., 2012).”
Background
Metadata
- Authors
- Leto, T. L., & Geiszt, M.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2006-09
- Volume
- 8
- Issue
- 9-10
- Pages
- 1549-1561
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W1997948093
- Cited by
- 254
- References
- 121
- FWCI
- 3.95
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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