Effect of rheumatoid factor and anti-immunoglobulin G antibodies on complement-mediated lysis of herpes simplex virus-infected human fibroblasts

Abstract

The effect of various anti-immunoglobulin G (IgG) antibodies on the complement-mediated lysis of herpes simplex virus-infected human fibroblasts was determined. IgM rheumatoid factor, a naturally occurring anti-human Fc, inhibited lysis, whereas rabbit anti-human IgG serum potentiated immune cytolysis. We attempted to explain this disparity by determining the effect various classess of anti-IgG's with differing specificities had on complement-mediated lysis. Inhibition of cytolysis occurred with IgM anti-Fc and all of the IgG antiglobulins (anti-IgG, Fab, and Fc). In contrast, IgM anti-Fab enhanced lysis. IgM anti-IgG suppressed immune cytolysis when high concentrations of antiviral serum were incubated with the virus-infected cell, but augmented lysis when low concentrations of anti-herpes simplex virus antibody were exposed to the fibroblasts. The experiments indicated that whether a particular antiglobulin potentiates or inhibits lysis depends on the concentration of antibody bound to the target cells as well as the class and specificity of the antiglobulin exposed to the antibody-coated cell.

Complement activation induced by rabbit rheumatoid factor

“…The presence of RF in hyperimmunized ani-mals and in certain disease states in humans suggests a biological function, and an immune stimulus may be common to these antibodies, potentially related to complement-associated reactions and immune complex disposal mechanisms. However, several studies have shown that, dependent upon the density of IgG on cell surfaces, human IgM RF can either enhance or inhibit complement activation and subsequent phagocytosis (23) or lysis (16,18,27,28). These data suggest that human IgM RF is relatively inefficient with regard to complement activation.…”