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pubmed-article:21641399pubmed:abstractTextMicrobial-induced inflammation is important for eliciting humoral immunity. Genetic defects of NADPH oxidase 2-based proteins interrupt phagocyte superoxide generation and are the basis for the human immunodeficiency chronic granulomatous disease (CGD). Hyperinflammation is also a significant clinical manifestation of CGD. Herein, we evaluated humoral immunity in the phagocyte oxidase p47(phox)-deficient model of CGD and found that UV-inactivated Streptococcus pneumoniae and Listeria monocytogenes (Lm) elicited higher specific antibody (Ab) titers in p47(phox-/-) mice than wild-type (WT) mice. Both organisms elicited robust and distinct antigen-presenting cell maturation phenotypes, including IL-12 hypersecretion, and higher major histocompatibility complex II and costimulatory protein expression in Lm-stimulated p47(phox-/-) dendritic cells (DCs) relative to WT DCs. Furthermore, p47(phox-/-) DCs pulsed with Lm and adoptively transferred into naïve WT mice elicited Ab titers, whereas Lm-pulsed WT DCs did not elicit these titers. The observed robust p47(phox-/-) mouse humoral response was recapitulated with live Lm and sustained in vivo in p47(phox-/-) mice. Notably, anti-serum samples from p47(phox-/-) mice that survived secondary Lm infection were protective in WT and p47(phox-/-) mice that were rechallenged with secondary lethal Lm infection. These findings demonstrate a novel benefit of NADPH oxidase 2 deficiency (ie, dependent inflammation in antigen-presenting cell-mediated humoral immunity) and that anti-Lm Ab can be protective in an immunodeficient CGD host.lld:pubmed
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pubmed-article:21641399pubmed:copyrightInfoPublished by Elsevier Inc.lld:pubmed
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pubmed-article:21641399pubmed:volume178lld:pubmed
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pubmed-article:21641399pubmed:year2011lld:pubmed
pubmed-article:21641399pubmed:articleTitleRole of p47phox in antigen-presenting cell-mediated regulation of humoral immunity in mice.lld:pubmed
pubmed-article:21641399pubmed:affiliationMolecular Trafficking Unit, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.lld:pubmed
pubmed-article:21641399pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21641399pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
pubmed-article:21641399pubmed:publicationTypeResearch Support, N.I.H., Intramurallld:pubmed
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