Toll receptor-mediated regulation of NADPH oxidase in human dendritic cells

Marisa Vulcano, Stefano Dusi, Daniele Lissandrini, Raffaele Badolato, Paola Mazzi, Elena Riboldi, Elena Borroni, Angelica Calleri, Marta Donini, Alessandro Plebani, Luigi Notarangelo, Tiziana Musso, Silvano Sozzani

Research output: Contribution to journalArticlepeer-review


Activation of NADPH oxidase represents an essential mechanism of defense against pathogens. Dendritic cells (DC) are phagocytic cells specialized in Ag presentation rather than in bacteria killing. Human monocyte-derived DC were found to express the NADPH oxidase components and to release superoside anions in response to phorbol esters and phagocytic-agonists. The NADPH oxidase components p47phox and gp91phox were down-regulated during monocyte differentiation to DC, and maturation of DC with pathogen-derived molecules, known to activate TLRs, increased p47phox and gp91 phox expression and enhanced superoxide anions release. Similar results were obtained with plasmacytoid DC following maturation with influenza virus. In contrast, activation of DC by immune stimuli (CD40 ligand) did not regulate NADPH oxidase components or respiratory burst. NADPH oxidase-derived oxygen radicals did not play any role in DC differentiation, maturation, cytokine production, and induction of T cell proliferation, as based on the normal function of DC generated from chronic granulomatous disease patients and the use of an oxygen radical scavenger. However, NADPH oxidase activation was required for DC killing of intracellular Escherichia coli. It is likely that the selective regulation of oxygen radicals production by pathogen-activated DC may function to limit pathogen dissemination during DC trafficking to secondary lymphoid tissues.

Original languageEnglish
Pages (from-to)5749-5756
Number of pages8
JournalJournal of Immunology
Issue number9
Publication statusPublished - Nov 1 2004

ASJC Scopus subject areas

  • Immunology


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