DISTRIBUTION OF A CROSS-REACTIVE IDIOTYPIC SPECIFICITY IN INBRED STRAINS OF MICE

The expression of an idiotype characteristic of anti-p-azophenylarsonate antibodies of all A/J mice was explored in F1 progeny, in other inbred strains, and in congenic mice. Of the strains tested only those closely related to A/J produced antibodies with the cross-reactive idiotype (CRI). None of the mice synthesized intermediate levels of CRI. No relationship between H-2 type and idiotype was noted. Congenic mice with a strain A background but a different H-2 type produced CRI in amounts quantitatively equivalent to those of strain A mice. Conversely, the presence of the H-2 genotype of strain A on an unrelated background was not associated with the formation of CRI. Nearly all F1 progeny of strain A mice formed CRI, indicating that failure of the other (non-A) parental strain to produce CRI is not attributable to the presence of a gene controlling the synthesis of a suppressor of CRI. NZB mice, which have the same heavy chain allotype as strain A, but are unrelated in origin, failed to produce CRI, although allotype has been shown to be linked to idiotype in congenic strains

REQUIREMENTS FOR PROLONGED SUPPRESSION OF AN IDIOTYPIC SPECIFICITY IN ADULT MICE

The appearance of an idiotypic specificity, present in anti-p-azophenylarsonate (anti-Ar) antibodies of all immunized A/J mice, ran be suppressed in adult mice by prior administration of an IgG fraction of rabbit antiidiotypic (anti-D) antiserum; anti-Ar antibodies arise but are of different idiotype. Prolonged suppression was observed in earlier experiments, but antigen was first administered to adult mice only 2 wk or 9 wk after anti-D antibodies; subsequent escape from idiotypic suppression could have been masked by the capture of antigen by large numbers of memory cells having receptors of a different idiotype. In the present experiments antigen was first administered at intervals up to 22 wk after the antiidiotypic antibody. Suppression was maintained for 6 wk in all mice and for 5 mo in about half the mice tested. It thus appears that suppression of idiotype is less reversible if antigen is administered soon after the antiidiotypic antibody. The data suggest that escape from suppression is attributable to the generation of new precursor cells rather than to reactivation of suppressed cells. The minimum dosage of antiidiotypic IgG required for effective suppression was about 2 mg. The subcutaneous or intraperitoneal routes of inoculation of antiidiotypic IgG were equally effective. When antiidiotypic antibody was administered 3 days after antigen no suppressive effects were observed. There was partial suppression when antiidiotypic antibody was injected on the same day as the antigen. Fab' and F(ab')2 fragments of antiidiotypic IgG had no suppressive effect. Quantitative measurements revealed no significant differences among control and suppressed mice with respect to total concentration of precipitable anti-Ar antibodies produced