{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Banki Z"],"funding":["Austrian Science Fund FWF","Deutsche Forschungsgemeinschaft"],"pagination":["E145"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6410291"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(2)"],"pubmed_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."],"journal":["Viruses"],"pubmed_title":["Fcγ Receptor Type I (CD64)-Mediated Impairment of the Capacity of Dendritic Cells to Activate Specific CD8 T Cells by IgG-opsonized Friend Virus."],"pmcid":["PMC6410291"],"funding_grant_id":["I-2550","Di714/17","P-21508","I 2550"],"pubmed_authors":["Stoiber H","Verbeek JS","Rossler A","Bayer W","Banki Z","Dittmer U","Werner R","Hegen V","Riepler L","Mullauer B"],"additional_accession":[]},"is_claimable":false,"name":"Fcγ Receptor Type I (CD64)-Mediated Impairment of the Capacity of Dendritic Cells to Activate Specific CD8 T Cells by IgG-opsonized Friend Virus.","description":"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.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Feb","modification":"2025-05-18T10:44:18.892Z","creation":"2025-05-18T10:44:18.892Z"},"accession":"S-EPMC6410291","cross_references":{"pubmed":["30744065"],"doi":["10.3390/v11020145"]}}