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Macrophage Death following Influenza Vaccination Initiates the Inflammatory Response that Promotes Dendritic Cell Function in the Draining Lymph Node

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Publication date 2017
Author Chatziandreou Nikolaos, Farsakoglu Yagmur, Palomino-Segura Miguel, D’Antuono Rocco, Pizzagalli Diego Ulisse, Sallusto Federica, Lukacs-Kornek Veronika, Uguccioni Mariagrazia, Corti Davide, Turley Shannon J., Lanzavecchia Antonio, Carroll Michael C., Gonzalez Santiago F.,
Project Acquisition of a 2-Photon microscope for intravital analysis
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Original article (peer-reviewed)

Journal Cell Reports
Volume (Issue) 18(10)
Page(s) 2427 - 2440
Title of proceedings Cell Reports
DOI 10.1016/j.celrep.2017.02.026

Open Access

URL https://www.ncbi.nlm.nih.gov/pubmed/28273457
Type of Open Access Website

Abstract

The mechanism by which inflammation influences the adaptive response to vaccines is not fully understood. Here, we examine the role of lymph node macrophages (LNMs) in the induction of the cytokine storm triggered by inactivated influenza virus vaccine. Following vaccination, LNMs undergo inflammasome-independent necrosis-like death that is reliant on MyD88 and Toll-like receptor 7 (TLR7) expression and releases pre-stored interleukin-1alpha (IL-1alpha). Furthermore, activated medullary macrophages produce interferon-beta (IFN-beta) that induces the autocrine secretion of IL-1alpha. We also found that macrophage depletion promotes lymph node-resident dendritic cell (LNDC) relocation and affects the capacity of CD11b+ LNDCs to capture virus and express co-stimulatory molecules. Inhibition of the IL-1alpha-induced inflammatory cascade reduced B cell responses, while co-administration of recombinant IL-1alpha increased the humoral response. Stimulation of the IL-1alpha inflammatory pathway might therefore represent a strategy to enhance antigen presentation by LNDCs and improve the humoral response against influenza vaccines.
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