During reinfection, high-affinity IgG Abs form complexes with both soluble Ag and Ag displayed on the surface of infected cells. These interactions regulate cellular activation of both innate cells and B cells, which express specific combinations of activating FcγRs (FcγRI, FcγRIII, FcγRIV) and/or the inhibitory FcγR (FcγRIIB). Direct proof for functional expression of FcγR by Ag-specific CD8 T cells is lacking. In this article, we show that the majority of memory CD8 T cells generated by bacterial or viral infection express only FcγRIIB, and that FcγRIIB could be detected on previously activated human CD8 T cells. Of note, FcγR stimulation during in vivo Ag challenge not only inhibited the cytotoxicity of memory CD8 T cells against peptide-loaded or virus-infected targets, but FcγRIIB blockade during homologous virus challenge enhanced the secondary CD8 T cell response. Thus, memory CD8 T cells intrinsically express a functional FcγRIIB, permitting Ag-Ab complexes to regulate secondary CD8 T cell responses.
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 08 April 2014.
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#15,330,127
of 22,800,560 outputs
Outputs from The Journal of Immunology
#16,016
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#190,187
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Outputs of similar age from The Journal of Immunology
#70
of 112 outputs
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