REGULATION OF TUMOR-GROWTH AND ANTIBODY CLONE EXPRESSION BY ANTIGEN AND ANTI-IDIOTYPE ANTIBODY LIGANDS WITH SPECIFICITY FOR RECEPTOR-BINDING SITES

Dextran ligands, modified to increase epitope reactivity with receptors, were more effective in suppressing BALB/c mouse plasmacytomas MOPC 104 E and J‐558, which bind α(1 → 3) dextran and have an idiotype (Id) in common, than autoantibody (Ab) against the Id unique to each of the proteins secreted by the two tumors (the Idl). BALB/c immunized with 104 E myeloma protein and expressing an antibody response to the 104 E Idl exhibited a specific, anti‐104E Idl transplantation resistance to lethal grafts of 104E, but not J‐558, tumors notwithstanding the shared common Id and similar ability to bind a(1 → 3) dextran. This autoantibody did not prevent modulation of the 104 E tumor to variant forms or the growth of the variants. On challenge with a(1 → 3) dextran, the immunized mice expressing the anti‐104E Idl responses failed to express the 104E Idl‐like antibody clone present in the normal, anti‐α(1 → 3) dextran antibody repertoire. Passive, iso‐anti‐104E Idl antibody had a transitory suppressive effect on the normal, 104E Idl‐like antibody clone but failed to circumvent 104 E tumor growth. It is apparent that the greater effectiveness of ligands strongly reactive in a nonphysiological manner with the tumor receptors lies in the stabilization of the tumor load without inducing variant escape or a disturbance of the immune network, and that receptor expression and malignancy state are not necessarily co‐extensive functions. Copyright © 1979 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim