A primary immune response to dextran B512 is followed by a period of antigen-specific immunosuppression caused by autoanti-idiotypic antibodies.

After a primary immune response to the alpha 1-6 epitope of dextran B512, dextran high responder strains exhibit a specific inability to produce IgM and IgG antibodies against this epitope, although they gave an expected secondary response to horse erythrocytes. Spleen cells from dextran-primed and-suppressed mice responded well to dextran after transfer to lethally irradiated previously untreated mice, indicating that tolerance or exhaustive proliferation of dextran reactive B cells is not responsible. Thymus-dependent dextran-protein conjugates also induced specific suppression. Suppression to both dextran and horse erythrocytes could be passively transferred into untreated recipients with immune serum. However, after absorption with horse erythrocytes and dextran, passive serum transfer only suppressed the response to dextran. It is suggested that the specific immunosuppression was caused by the appearance of autoanti-idiotypic antibodies directed against the immunoglobulin receptors of dextran-reactive B cells.