B cell chimerism was analyzed in juvenile chickens given injections of major histocompatibility complex-compatible lymphoid cells. The allelic products of donor and host-derived B cells were monitored with antisera directed against M1 (IgM) and G1 (IgG) isotype-specific allotypes. Injection of peripheral blood lymphocytes and spleen cells suppressed host allotype levels whereas purified T lymphocytes were ineffective. Pre-treatment of recipients with cyclophosphamide was more effective than irradiation in promoting both engraftment and host B cell suppression. Host allotype suppression endured for several months after cell transfer and was attributable to B cell deletion, as ascertained by the lack of cells which expressed surface M1. In partially suppressed chickens, host G1 was inhibited to a greater degree than M1 allotype. Host recovery was followed by donor B cell rejection when low numbers of donor cells and/or inadequate host conditioning was used. Selective M1 chimerism occurred when limiting numbers of spleen cells were transferred into cyclophosphamide-treated hosts, whereas selective G1 chimerism resulted after the transfer of large numbers of peripheral blood lymphocytes or spleen cells into unconditioned recipients. We consider that these findings can be attributed to a B cell surveillance mechanism which may be similar to that postulated previously to explain resistance to haemopoietic and tumour cells.