Monolayers of mouse embryo fibroblasts were labeled with51Cr and infected with vaccinia virus. When sequentially incubated with rabbit antivaccinial antibody and excess guinea pig complement, the fibroblasts lysed and liberated51Cr into the medium. The51Cr released was proportional to the antiviral antibody concentration incubated with the cells. When the infected cells were treated with antibody and exposed to125I-labeled human rheumatoid factor (RF), the labeled antiglobulin bound to the antiviral antibody on the virus-infected cells. The effect of RF and goat anti-rabbit IgG on complement-mediated lysis was determined. When high concentrations of antiviral antibody were incubated with the infected cells both RF and anti-rabbit IgG inhibited complement-mediated cytolysis. At low concentration of antibody, RF had no effect on immune lysis, while anti-rabbit IgG enhanced lysis. This is a hitherto unrecognized role of RF and suggests that RF in vivo may alter the humorally mediated immune cytolysis of virus-infected cells. © 1975.
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