1. Cellular receptors, differentiation and endocytosis requirements are key factors for type I IFN response by human epithelial, conventional and plasmacytoid dendritic infected cells by measles virus.
- Author
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Duhen T, Herschke F, Azocar O, Druelle J, Plumet S, Delprat C, Schicklin S, Wild TF, Rabourdin-Combe C, Gerlier D, and Valentin H
- Subjects
- Antigens, CD immunology, Cells, Cultured, Dendritic Cells cytology, Dendritic Cells virology, Epithelial Cells cytology, Epithelial Cells virology, Humans, Measles physiopathology, Measles virology, Measles virus genetics, Measles virus immunology, Membrane Cofactor Protein immunology, Receptors, Cell Surface immunology, Signaling Lymphocytic Activation Molecule Family Member 1, Viral Tropism, Cell Differentiation, Dendritic Cells immunology, Endocytosis, Epithelial Cells immunology, Interferon Type I immunology, Measles immunology, Measles virus physiology, Receptors, Virus immunology
- Abstract
While the antiviral response during measles virus (MeV) infection is documented, the contribution of the hosting cell type to the type I interferon (IFN-alpha/beta) response is still not clearly established. Here, we report that a signature heterogeneity of the IFN-alpha/beta response according to the cell type. The MeV tropism dictated by the expression of appropriate cellular receptor appeared to be crucial for epithelial cells. For conventional DCs (cDCs), the maturation state played a prominent role. In response to both wild type MeV isolates and laboratory/vaccine strains, immature cDCs produced higher levels of IFN-alpha than mature cDCs, despite the reduced expression levels of both CD46 and CD150 receptors by the former ones. While in epithelial cells and cDCs the MeV transcription was required to activate the IFN-alpha/beta response, plasmacytoid DCs (pDCs) rapidly produced large amounts of IFN-alpha mostly independently of the viral infection cycle. This argues for a significant contribution of pDCs in response to MeV infection and/or vaccination., (Copyright (c) 2010 Elsevier B.V. All rights reserved.)
- Published
- 2010
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