Induction of passive cutaneous anaphylaxis in monkeys by human γE antibody

Serum and serum fractions from ragweed-sensitive patients were tested for their ability to induce passive cutaneous anaphylaxis (PCA) in Macaca irus. When purified ragweed allergen (antigen E) was used, the ability of the samples to induce the PCA reactions paralleled their skin-sensitizing activity in Prausnitz-Küstner reactions in humans and correlated with the concentration of γE antibody as measured by allergen-binding activity. The titer of the samples in the PCA reactions bore no correlation with either γG or γA antibody level. The allergen-binding activity of γE antibody in six different samples containing the minimal amount required to give positive PCA reactions was of the order of 0.00015 to 0.00035 mcg. of antigen E. This dose of the antibody is equivalent to 5×10^-5 mcg.N of rabbit antibody to the same antigen, with respect to allergen-binding activity. One thousand times as much γG antibody and 20 times as much γA antibody were incapable of inducing a positive PCA reaction. The presence of excess γG antibody in the γE antibody-containing samples for sensitization neither prevented nor enhanced the PCA reaction. The skin-sensitizing activity of a patient's serum and its reagin-rich fraction were lost by the precipitation of γE-globulin, whereas the precipitation of γA- and γG-globulins in the fraction did not diminish the activity. These findings indicate that γE antibody is responsible for the PCA reactions in monkeys. It was also found that as much as 1 mcg.N of rabbit γG antibody to antigen E did not give PCA reactions in monkeys, whereas 0.003 mcg.N of the antibody was sufficient to give the reactions in guinea pigs.