Superoxide anions induce the maturation of human dendritic cells.

Détails

ID Serval
serval:BIB_1ECC715BACF9
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Superoxide anions induce the maturation of human dendritic cells.
Périodique
American Journal of Respiratory and Critical Care Medicine
Auteur(s)
Kantengwa S., Jornot L., Devenoges C., Nicod L.P.
ISSN
1073-449X[print], 1073-449X[linking]
Statut éditorial
Publié
Date de publication
2003
Volume
167
Numéro
3
Pages
431-437
Langue
anglais
Résumé
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)-kappaB, 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-kappaB 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-kappaB-dependent mechanism.
Mots-clé
Cells, Cultured, Dendritic Cells/drug effects, Dendritic Cells/physiology, Humans, Reactive Oxygen Species/immunology, Superoxides/immunology, Xanthine/antagonists & inhibitors, Xanthine/pharmacology, Xanthine Oxidase/antagonists & inhibitors, Xanthine Oxidase/pharmacology
Pubmed
Web of science
Création de la notice
19/02/2010 20:07
Dernière modification de la notice
03/03/2018 14:36
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