No abstract

Pepsin-digested rabbit antibody (5S) provoked reverse passive cutaneous anaphylaxis in the guinea pig, but was somewhat less effective, mole for mole, than the native antibody. Fixation of guinea pig complement by the pepsin-digested antibody could not be demonstrated either in vitro or in vivo. Splitting of the 5S fragment into two monovalent fragments (3.5S) markedly reduced the capacity to provoke reverse passive cutaneous anaphylaxis.

High titer and persistent antihapten IgE production in SJL mice can be obtained using appropriate immunization and radiation. Nonirradiated mice rapidly terminate this antihapten IgE production. Radiation was not necessary to prolong antihapten IgE production in other strains of mice. Termination can be obtained even in irradiated SJL mice by transferring normal SJL spleen cells. That the suppressor cells are T cells is shown by using thymocytes or cells treated with anti-Thy 1.2 and complement. No appreciable suppressive effect by normal spleen cells could be demonstrated on IgG1 production in SJL mice. The characteristic of low and transient IgE antibody response in SJL mice is inherited as a recessive trait controlled by a single Mendelian autosomal gene and is not linked to the H-2-gene complex. This characteristic does not depend on the infectivity of Nippostrongylus brasiliensis, the effect of anticarrier antibody, or the recognition of antigen.

Mouse IgE was titrated in rats. The sensitization period was 2h. The results were consistent and corresponded to the titers obtained in young adult SJL mice using a sensitization period of 48 h. With longer sensitization periods in rats, higher antibody titers were obtained. The optimum sensitization period in rats was found to be 48 h. Old CFW mice are inadequate for mouse IgE titration. IgG₁ will not give a PCA reaction in rats. IgG₁ titers are higher in SJL or A/J mice than in young CFW mice, and markedly higher than in old CFW mice.

Although penicillin G (PG) 1 has long been known to be a clinical allergen, the identity of the antigenic determinant groups responsible for hypersensitivity to P G is not clearly known. Such knowledge would be of importance since it would lead to the preparation of conjugated protein antigens useful as reagents to diagnose penicillin hypersensitivity. This information would make possible also the synthesis of low molecular weight univalent haptens which might be useful, therapeutically, to specifically inhibit antibody-dependent penicillin allergic reactions. Also, with the clear definition of the responsible antigenic determinant groups, the penicillin system m a y be employed as a model to study more general problems of human hypersensitivity.