Mitochondrial reactive oxygen species regulate the induction of CD8+ T cells by plasmacytoid dendritic cells

Marine Oberkampf, Camille Guillerey, Juliette Mouriès, Pierre Rosenbaum, Catherine Fayolle, Alexandre Bobard, Ariel Savina, Eric Ogier-Denis, Jost Enninga, Sebastian Amigorena, Claude Leclerc () and Gilles Dadaglio ()
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Marine Oberkampf: Equipe Labellisée Ligue Contre le Cancer
Camille Guillerey: Equipe Labellisée Ligue Contre le Cancer
Juliette Mouriès: Equipe Labellisée Ligue Contre le Cancer
Pierre Rosenbaum: Equipe Labellisée Ligue Contre le Cancer
Catherine Fayolle: Equipe Labellisée Ligue Contre le Cancer
Alexandre Bobard: Dynamique des Interactions Hôte-Pathogène
Ariel Savina: Institut Curie
Eric Ogier-Denis: Faculté de Médecine Xavier Bichat
Jost Enninga: Dynamique des Interactions Hôte-Pathogène
Sebastian Amigorena: Institut Curie
Claude Leclerc: Equipe Labellisée Ligue Contre le Cancer
Gilles Dadaglio: Equipe Labellisée Ligue Contre le Cancer

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Cross-presentation allows exogenous antigen presentation in association with major histocompatibility complex class I molecules, a process crucial for the priming of CD8+ T-cell responses against viruses and tumors. By contrast to conventional dendritic cells (cDC), which cross-present antigens in the steady state, plasmacytoid dendritic cells (pDC) acquire this ability only after stimulation by Toll-like receptor (TLR) ligands. The intracellular pathways accounting for this functional difference are still unknown. Here we show that the induction of cross-presentation by pDCs is regulated by mitochondria through a reactive oxygen species (ROS)-dependent mechanism, involving pH alkalization and antigen protection. The reduction of mitochondrial ROS production dramatically decreases the cross-presentation capacity of pDCs, leading to a strong reduction of their capacity to trigger CD8+ T-cell responses. Our results demonstrate the importance of mitochondrial metabolism in pDC biology, particularly for the induction of adaptive immune responses.

Date: 2018
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04686-8

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DOI: 10.1038/s41467-018-04686-8

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