Human Cytomegalovirus Induces an Fe Receptor (Fc R) in Endothelial Cells and Fibroblasts that Is Distinct from the Human Cellular Fc Rs

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Abstract
The expression of a trypsin-sensitive receptor for the Fe portion of IgG (FcγR) was demonstrated by flow cytometry on the surface of human umbilical vein endothelial cells and fibroblasts infected with human cytomegalovirus (CMV). Double-labeling experiments showed strong expression of the CMV FCyR in a perinuclear region of infected cells but not in bystander un infected cells. The CMV FCyRdid not react with a panel of murine monoclonal antibodies directed against the known human IgG Fe receptors, FCγRI, FCγRII, and FCγRIII. The cytoplasmic form but not the cell surface form of CMV FCγR bound murine IgG3 moderately and murine IgGl more weakly, while both forms bound rabbit IgG almost as strongly as human IgG. The function of CMV FCγR is unclear, but it may allow CMV to evade host antibody responses. However, the binding of immune complexes to infected endothelium might also contribute to immunopathology.

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