1. Fcγ Receptor Type I (CD64)-Mediated Impairment of the Capacity of Dendritic Cells to Activate Specific CD8 T Cells by IgG-opsonized Friend Virus.
- Author
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Bánki Z, Werner R, Riepler L, Rössler A, Müllauer B, Hegen V, Bayer W, Verbeek JS, Dittmer U, and Stoiber H
- Subjects
- Animals, Antigen Presentation, Antigen-Antibody Complex immunology, Dendritic Cells virology, Immunoglobulin G immunology, Mice, Mice, Inbred C57BL, Receptors, IgG genetics, CD8-Positive T-Lymphocytes immunology, Dendritic Cells immunology, Friend murine leukemia virus immunology, Lymphocyte Activation, Receptors, IgG immunology
- 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.
- Published
- 2019
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