Cross-talk between human dendritic cell subsets influences expression of RNA sensors and inhibits picornavirus infection.
Publication year
2010Source
Journal of Innate Immunity, 2, 4, (2010), pp. 360-370ISSN
Publication type
Article / Letter to editor

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Organization
Tumorimmunology
Paediatrics - OUD tm 2017
Medical Oncology
Medical Microbiology
Journal title
Journal of Innate Immunity
Volume
vol. 2
Issue
iss. 4
Page start
p. 360
Page end
p. 370
Subject
N4i 1: Pathogenesis and modulation of inflammation; NCMLS 1: Infection and autoimmunity; NCMLS 2: Immune RegulationAbstract
Dendritic cells (DCs) are professional antigen-presenting cells that provide a link between innate and adaptive immunity. Multiple DC subsets exist and their activation by microorganisms occurs through binding of conserved pathogen-derived structures to so-called pattern recognition receptors (PRRs). In this study we analyzed the expression of PRRs responding to viral RNA in human monocyte-derived DCs (moDCs) under steady-state or pro-inflammatory conditions. We found that mRNA and protein levels for most PRRs were increased under pro-inflammatory conditions, with the most pronounced increases in the RIG-like helicase (RLH) family. Additionally, freshly isolated human plasmacytoid DCs (pDCs) displayed significantly higher levels of TLR7, RIG-I, MDA5 and PKR as compared to myeloid DCs and moDCs. Finally, we demonstrate for the first time that cross-talk between TLR-matured or virus-stimulated pDCs and moDCs leads to a type I interferon-dependent antiviral state in moDCs. This antiviral state was characterized by enhanced RLH expression and protection against picornavirus infection. These findings might represent a novel mechanism by which pDCs can preserve the function and viability of myeloid DCs that are attracted to a site with ongoing infection, thereby optimizing the antiviral immune response.
This item appears in the following Collection(s)
- Academic publications [203793]
- Electronic publications [102109]
- Faculty of Medical Sciences [80320]
- Open Access publications [70806]
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