Carrier-induced suppression of the antibody response to a 'self' hapten.

Immunization of male rats and monkeys with gonadotropin-releasing hormone (GnRH) conjugated to a carrier results in a dramatic atrophy of the prostate. GnRH, linked to either diphtheria toxoid or tetanus toxoid as carrier, is now being evaluated for its use in the immunotherapy of hormone-dependent prostate enlargement in men. This report deals with the phenomenon of carrier-induced, epitope-specific regulation in the GnRH-carrier system. In experiments designed to assess the influence of the carrier on antibody responses to the 'self' hapten GnRH, we show that preimmunization with carriers diphtheria toxoid and tetanus toxoid results in a strain-dependent inhibition of anti-GnRH responses in mice. Results of adoptive transfer experiments indicate that T cells from carrier-presensitized mice are responsible for suppression of anti-haptenic antibodies and that T cells from conjugate-immunized mice, on the other hand, can actually help overcome hyporesponsiveness.