Isogeneic monoclonal antibodies against anti-alpha(1----3)dextran idiotypes. I. Isotypes, idiotope specificity and representation of idiotopes in antisera from mice of various genetic constitutions.

Eight isogeneic anti-idiotypic hybridomas were raised against BALB/c myeloma protein MOPC 104E and one against J558. Both myelomas react specifically with the alpha(1----3) glucosidic linkage of dextran B1355 fraction S (Dex). Six anti-MOPC 104E proteins were IgG1, one was IgG2b and one IgM. The anti-J558 protein was IgG1. Competitive interactions of the anti-idiotopes and antigen with anti-Dex proteins were measured. Dex itself was effective, but also an alpha(1----3) glucosidic heptasaccharide (N7-CHO). In order to assess the anti-idiotope specificity of hybridoma proteins, three anti-Dex molecules were used: MOPC 104E, J558 and hybridoma protein Hdex14. These differed from each other in VH amino acid positions 54-55, or 100-101, respectively. By their serological reaction pattern our anti-idiotope proteins could be divided into 3 groups: cross-reactive, partially cross-reactive and strictly specific for the immunogen. The latter ones were in the majority, and were called "private", in contrast to the cross-reactive "public" anti-idiotopes. The serological pattern was followed, in general, by the mouse-to-mouse distribution of idiotopes in physiological anti-Dex sera. Public idiotopes were closely correlated in their expression with anti-Dex activity. "Private" idiotopes showed no correlation, and displayed a characteristically high degree of fluctuation from mouse to mouse. Among the different mouse strains that were compared with respect to idiotope expression in anti-Dex sera, two stand out: C57BL-Igha, which carries chromosome 12 of BALB/c, (as selected through allotype) on the C57BL/6 genome, and BALB-Ighb, dex+, a recombinant in chromosome 12 linking the dex+ trait from BALB/c to the CH allotype from C57BL/6. The latter strain expressed significantly more of the private idiotopes than the former. This observation is discussed in terms of the position effect of classical genetics and network concepts.