The intravenous administration to mice of soluble antigen-antibody complexes in antigen excess resulted in a high incidence of glomerulonephritis and less frequently in endocarditis or arteritis. These lesions are present within 48 hours of the first of 3 injections and disappear within 2 weeks.
The same pathological changes were produced with complexes prepared from either rabbit or chicken antibody. In the case of rabbit antibody, the severity of the glomerulonephritis was greater with the ovalbumin antiovalbumin system than with the BSA system.
Anaphylaxis regularly occurred in mice given complexes prepared from rabbit antibody, but was not seen following administration of complexes prepared from chicken antibody.
Pretreatment with cortisone diminished the severity of the glomerulo-nephritis and resulted in accumulation of amorphous, eosinophilic material within glomerular capillaries in mice injected with antigen-antibody complexes.
The rabbit antibody used in these experiments failed to sensitize guinea pig skin to passive cutaneous anaphylaxis when injected in the form of soluble complexes. This indicates that these complexes do not dissociate to a detectable extent in vivo and thus favors the interpretation that complexes localize as such in the sites where tissue damage occurs.
Chicken anti-mouse erythrocyte antibody produced hemolysis of mouse red cells in the presence of mouse complement. In contrast to a similar rabbit anti-serum, the hemolytic activity of the chicken antibody with mouse complement was very slight. This suggests that complement does not play an important role in the pathogenesis of these experimental lesions.