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Superoxide Anions Induce the Maturation of Human Dendritic Cells

Divisions of Pneumology and Thoracic Surgery, University Hospital, Geneva, Switzerland

Correspondence and requests for reprints should be addressed to Dr. Salomé Kantengwa, Division of Pneumology, University Hospital of Geneva, 24 rue Micheli-du-Crest, CH-1211 Geneva 14, Switzerland. E-mail: Salome.Kantengwa{at}hcuge.ch

Dendritic cells play a key role in immune responses. There is growing evidence that reactive oxygen species participate in signaling pathways involving nuclear factor (NF)-B, leading to expression of important immune system genes. We found that, unlike H₂O₂, reactive oxygen species generated by the reaction of oxidase on xanthine induced early phenotypic maturation of dendritic cells by upregulating specific markers CD80, CD83, and CD86 and downregulating mannose receptor–mediated endocytosis. Maturation induced by xanthine oxidase was prevented by allopurinol, an inhibitor of xanthine oxidase activity, and by N-acetylcysteine. The proteasome inhibitor MG-132, which blocks NF-B activation, also inhibited CD86 upregulation, but not endocytosis downregulation by reactive oxygen species. Finally, xanthine-xanthine oxidase enhanced or blocked antigen presentation by dendritic cells depending on whether they had been prepulsed or not with the antigen. Taken together, these results demonstrate that oxidative stress induces phenotypic and functional maturation of dendritic cells, partly through an NF-B–dependent mechanism.

Key Words: reactive oxygen species • dendritic cell • maturation

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