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A role for NADPH oxidase in antigen presentation

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FRONTIERS IN IMMUNOLOGY
卷 4, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2013.00295

关键词

NADPH oxidase; B lymphocytes; chronic granulomatous disease; autoimmunity; antigen presentation

资金

  1. National Institutes of Health [R01 AI079065]
  2. Indiana CTSI
  3. Merilyn Hester Scholarship Fund
  4. NIH [T32 DK007519, T32 AI060519]
  5. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI060519, R01AI079065] Funding Source: NIH RePORTER
  6. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [T32DK007519] Funding Source: NIH RePORTER

向作者/读者索取更多资源

The nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expressed in phagocytes is a multi-subunit enzyme complex that generates superoxide (O-2(center dot-)). This radical is an important precursor of hydrogen peroxide (H2O2) and other reactive oxygen species needed for microbicidal activity during innate immune responses. Inherited defects in NADPH oxidase give rise to chronic granulomatous disease (CGD), a primary immunodeficiency characterized by recurrent infections and granulomatous inflammation. Interestingly, CGD, CGD carrier status, and oxidase gene polymorphisms have all been associated with autoinflammatory and autoimmune disorders, suggesting a potential role for NADPH oxidase in regulating adaptive immune responses. Here, NADPH oxidase function in antigen processing and presentation is reviewed. NADPH oxidase influences dendritic cell (DC) crosspresentation by major histocompatibility complex class I molecules through regulation of the phagosomal microenvironment, while in B lymphocytes, NADPH oxidase alters epitope selection by major histocompatibility complex class II molecules.

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