Antibody-activated immunoregulatory T cells are defective in B cell deprived mice.

We have previously shown that antibody bound to hapten-conjugated macrophages influences the contact sensitivity response to the hapten, the effect depending upon the isotype of antibody used. In the present experiments, we have examined the regulation of the contact sensitivity response of mice lacking B cells, in order to determine whether B cells and/or their products play a role in regulating such responses in situ. We have observed that contact sensitivity is normally induced in such B cell depleted mice, in contrast to the previously described failure of such mice to mount proliferative T cell responses to protein antigens. However, virtually all of the immunoregulatory activities previously defined in the contact sensitivity reaction, including those induced by antibody bound to hapten-coupled macrophages, cannot be elicited in these animals. In particular, intravenous injection of either hapten-coupled PEC, or antigen-antibody complexes of the IgG2a isotype on the surface of a hapten-coupled PEC (both of which induce unresponsiveness to contact sensitization in normal mice due to the activation of suppressor T cell activity) actually sensitize B cell deficient mice. Thus, we conclude that B cells or their products play a central role in the development and/or functioning of immunoregulatory cells involved in the control of contact sensitivity responses.