Next Article in Journal
A New Genotype of Feline Morbillivirus Infects Primary Cells of the Lung, Kidney, Brain and Peripheral Blood
Next Article in Special Issue
Lipid Exchange Factors at Membrane Contact Sites in African Swine Fever Virus Infection
Previous Article in Journal
Human Sapovirus among Outpatients with Acute Gastroenteritis in Spain: A One-Year Study
Previous Article in Special Issue
Monitoring HIV-1 Assembly in Living Cells: Insights from Dynamic and Single Molecule Microscopy
Article Menu
Issue 2 (February) cover image

Export Article

Open AccessArticle
Viruses 2019, 11(2), 145; https://doi.org/10.3390/v11020145

Fcγ Receptor Type I (CD64)-Mediated Impairment of the Capacity of Dendritic Cells to Activate Specific CD8 T Cells by IgG-opsonized Friend Virus

1
Division of Virology, Medical University of Innsbruck, Innsbruck, 6020, Austria
2
Institute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany
3
Department of Human Genetics, Leiden University Medical Center, Leiden, the Netherlands
*
Author to whom correspondence should be addressed.
Current address: Toin University of Yokohama, Department of Medical Engineering, Yokohama, Japan
Received: 16 November 2018 / Revised: 31 January 2019 / Accepted: 1 February 2019 / Published: 8 February 2019
(This article belongs to the Special Issue Breakthroughs in Viral Replication)
Full-Text   |   PDF [2239 KB, uploaded 8 February 2019]   |  

Abstract

Dendritic cells (DCs) express Fcγ receptors (FcγRs) for the binding immune complexes (ICs) consisting of IgG and antigens (Ags). IC–FcγR interactions have been demonstrated to enhance activation and antigen-presenting functions of DCs. Utilizing Friend virus (FV), an oncogenic mouse retrovirus, we investigated the effect of IgG-opsonization of retroviral particles on the infection of DCs and the subsequent presentation of viral antigens by DCs to virus-specific CD8 T cells. We found that opsonization by virus-specific non-neutralizing IgG abrogated DC infection and as a consequence significantly reduced the capacity of DCs to activate virus-specific CD8 T cells. Effects of IgG-opsonization were mediated by the high-affinity FcγR type I, CD64, expressed on DCs. Our results suggest that different opsonization patterns on the retroviral surface modulate infection and antigen-presenting functions of DCs, whereby, in contrast to complement, IgG reduces the capacity of DCs to activate cytotoxic T cell (CTL) responses. View Full-Text
Keywords: friend virus; dendritic cells; IgG-opsonization; Fcγ receptors; CD8 T cells friend virus; dendritic cells; IgG-opsonization; Fcγ receptors; CD8 T cells
Figures

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material

SciFeed

Share & Cite This Article

MDPI and ACS Style

Bánki, Z.; Werner, R.; Riepler, L.; Rössler, A.; Müllauer, B.; Hegen, V.; Bayer, W.; Verbeek, J.S.; Dittmer, U.; Stoiber, H. Fcγ Receptor Type I (CD64)-Mediated Impairment of the Capacity of Dendritic Cells to Activate Specific CD8 T Cells by IgG-opsonized Friend Virus. Viruses 2019, 11, 145.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top