Activation of Complement by Tetrathyridia of Mesocestoides corti: Enhancement by Antibodies from Infected Mice and Lack of Effect on Parasite Viability

Abstract

Tetrathyridia of the cestode Mesocestoides corti were isolated from the peritoneal cavity of infected mice. The parasites activated guinea pig and mouse complement (C) in vitro by both the classical and alternative pathways as shown by quantitative C fixation and crossed immunoelectrophoresis. The ability of tetrathyridia to activate mouse C was enhanced by preincubating the parasites in serum obtained from mice infected with M. corti. Antibodies of the IgG1 class, an immunoglobulin found in profoundly increased amounts in mice infected with M. corti, as well as IgM and IgG2 antibodies, bound to cultured tetrathyridia and facilitated deposition of the third component of C (C3) from dilute mouse serum, presumably via classical pathway activation. The results demonstrate that mouse IgG1 antibodies do not prevent the activation of C by the tetrathyridia or by C-fixing antibodies of other classes which become attached to the tetrathyridia. The activation of C in vitro by tetrathyridia did not affect their ability to grow in mice, even though C3-derived polypeptides could be detected by immunofluorescence on the surface of the parasites.

Phagocytosis inMesocestoides vogae-induced peritoneal monocytes/macrophages via opsonin-dependent or independent pathways

“…Indeed, it was shown that macrophages and giant cells from granulomas loose their receptors, particularly those for IgG (Mariano et al, 1977). Toye et al (1984) revealed that activation of complement did not play an essential role in the restriction of M. vogae growth in mice, indirectly supporting our fi ndings. We further evaluated the capacity of naive and post-infection peritoneal macrophages and monocytes to internalize non-opsonized particles.…”