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Abstract
Plasmacytoid dendritic cells (pDC) are specialized in secretion of type I interferon in response to pathogens. Here we show that natural monoamines and synthetic amines inhibit pDC activation by RNA viruses. Furthermore, a synthetic analogue of histamine reduces type I interferon production in a mouse model of influenza infection. We identify CXC chemokine receptor 4 (CXCR4) as a receptor used by amines to inhibit pDC. Our study establishes a functional link between natural amines and the innate immune system and identifies CXCR4 as a potential ‘on-off’ switch of pDC activity with therapeutic potential.
Highlights
Plasmacytoid dendritic cells are specialized in secretion of type I interferon in response to pathogens
CB strongly inhibited IFN-a production (Fig. 1g) and membrane TNF-related apoptosis inducing ligand (TRAIL) expression (Fig. 1h) by Plasmacytoid dendritic cells (pDC) cultured with Influenza and Dengue viruses, demonstrating that CB effect was not restricted to human immunodeficiency virus type 1 (HIV-1)
Plasmacytoid dendritic cells are innate immune cells implicated in multiple diseases because of their capacity of secreting massive levels of type I interferon, in particular IFN-a
Summary
Plasmacytoid dendritic cells (pDC) are specialized in secretion of type I interferon in response to pathogens. We show that natural monoamines and synthetic amines inhibit pDC activation by RNA viruses. Plasmacytoid dendritic cells (pDC) are the first line of host defence against viruses and bacteria[1] and link innate to adaptive immunity[2]. These immune cells are activated after recognition of pathogen nucleic acids by sensors such as Toll-like receptors (TLR). The modulation of pDC activation is only partly documented Synthetic molecules such as chloroquine[10], rapamycin[17] or antiBDCA-2 antibodies[18] decrease type I interferon production through various mechanism. The atopic phenotype in children, characterized by hyperhistamine secretion, is associated with a reduction in virusinduced interferon-a (IFN-a) release[21]
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