In vivo suppression of perinatal multispecific B cells results in a distortion of the adult B cell repertoire.

The isolation of multispecific B cell hybridomas with a variety of anti-idiotype (anti-Id) activities from the lymphoid organs of fetal and neonatal BALB/c mice suggested that the development of the immune system may depend on Id interactions among autologous B cells. In vitro analysis of antibodies secreted by these hybridomas showed extensive sharing of an idiotope defined by the monoclonal antibody FD5-1. Early and timed administration of this antibody during the perinatal period results in a distortion of the phosphorylcholine (PC) and alpha (1----3)dextran (Dex)-specific B cell precursor compartment of the developing repertoire and is reflected by a drastic reduction of antibody responses to these antigens when challenged as adults. These observations provide strong evidence for the involvement of the early appearing multispecific B cells in Id interactions that bring about the uniform development of the normal adult B cell repertoire. Interference with these interactions at critical stages of developmental results in permanent deficiencies in the adult B cell repertoire.