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In this article, L. Saveanu’s team, in collaboration with R. Monteiro and J. El Benna, demonstrated that FcγR-mediated uptake by type 2 and inflammatory DC subsets mediates antibody-dependent cross-presentation and activation of CD8+ T cell responses. They demonstrated an important role for the p84 regulatory subunit of PI3Kγ in this process. FcγR-mediated cross-presentation on type 2 and inflammatory DCs depends on the enzymatic activity of the p84/p110γ complex of PI3Kγ, which controls the activity of the NADPH oxidase NOX2 and ROS production in murine spleen type 2 DCs and GM-CSF-derived inflammatory DCs. In contrast, p84/p110γ is largely dispensable for cross-presentation by type 1 DCs. These findings suggest that PI3Kγ-targeted therapies currently under consideration for oncological practice may interfere with the ability of type 2 and inflammatory DCs to cross-present antigens contained in immune complexes.
