Regulation of anti-hapten antibody response by chemically modified carrier antigen preferentially provoking delayed-type hypersensitivity. I. Possible T-T cell interaction in the suppression of antibody response

Abstract

The i.p. immunization with chemically modified antigen (dodecanoyl-bovine serum albumin, d-BSA) emulsified in Freund's incomplete adjuvant (FIA) of CBA mice provoked delayed-type hypersensitivity (DTH), but not any detectable formation of antibody to the original antigen (BSA). Furthermore, it was found that immunization with d-BSA could generate T cells capable of inhibiting the antibody response to hapten on BSA, and the immunosuppressive effects of these T cells were presumably not due to direct action on hapten-primed and antibody producing B cells. These results were obtained from the following experiments: (1) anti-hapten antibody response to dinitrophenylated-BSA (DNP-BSA) was inhibited when the mice had been primed previously with d-BSA in FIA. This inhibition was regulated by the specificity of the carrier, since the mice treated with d-BSA did not inhibit the anti-DNP antibody response after the immunization with DNP-heterologous carrier, i.e. DNP-keyhole limpet haemocyanin (DNP-KLH). (2) The passive transfer of spleen cells, which had been obtained from donors primed with d-BSA in FIA, inhibited the primary anti-DNP antibody response of syngeneic mice after immunization with DNP BSA. (3) Injection of d-BSA-primed spleen cells suppressed an adoptive anti-DNP antibody response in mice which had been irradiated and had previously had their immunocompetence reconstituted by the cell transfers with both DNP-primed and BSA-primed spleen cells. This in vivo immunosuppressive effect of d-BSA-primed spleen cells did not act on hapten-primed B cells, since d-BSA-primed spleen cells could not suppress the adoptive secondary antibody response reconstituted by DNP-primed cells and bacterial alpha-amylase (BαA)-primed cells. This finding suggests that a T—T cell interaction exists for the suppression of the anti-DNP antibody response to DNP-BSA by d-BSA-primed cells.