It has previously been shown that there are extensive idiotypic cross-reactions among antiphenylarsonate antibodies of A/J mice. The present work indicates that administration, into normal, adult A/J mice, of rabbit antiidiotypic antibody directed to A/J antiphenylarsonate antibody suppresses almost completely the subsequent production of antibody of the corresponding idiotype. No effect was noted on the formation of antibodies to the protein carrier or of antiphenylarsonate antibody of a different idiotype. The data are consistent with central suppression of production of the idiotypic antibody mediated through interaction with immunoglobulin receptors on lymphocytes.

Rabbit anti-idiots~ic antisera specific for anti-p-azophenylarsonate (antiAr) t antibodies, raised in an individual strain A / J mouse, recognize determinants on anti-Ar antibodies induced in all members of this strain so far tested. These determinants have been found only on anti-At antibodies and not on normal imnmnoglobulins or on other anti-hapten or anti-protein antibodies induced in this strain (1-3). 2 The determinants on A/J anti-Ar antibodies are thus idiotypic and cross-reactive within the strain. In contrast, anti-Ar antibodies induced in most but not all other strains of mice (1, 3; Pawlak and Nisonoff, manuscript in preparation), lack the cross-reactive A/J idiotypic determinant. For this reason the idiotype of A/J anti-Ar antibody is potentially a genetic marker (phenotype).We report here finding the A/J idiotype on anti-Ar antibodies induced in strain AL/N mice; this strain was derived from an outcrossed strain A mouse (4). Strains AL/N and A/J share a number of characteristics, including similar H-2 complex loci (4) and most but not all IgCH allotypic determinants (5, 6), which are localized to the Fc fragment of the molecule. Strain AL/N then probably shares many genes with strain A/J but, according to Staats (4) cannot be considered a true subline of strain A (4).The presence of the cross-reactive idiotypic determinants on anti-Ar antibodies induced in strain AL/N mice is particularly fortuitous because we have recently completed, at the National Institutes of Health, the development of a congenic strain of BALB/c mice,