SUMMARY The quantitative relationship between donor and host allotype synthesis was studied in B cell chimeric chickens. Juvenile, cyclophosphamide-treated B14A strain, or (B14A x CHA)F1 hybrid recipients were given injections of spleen, bone marrow, or bursal cells from B14C donors and serum IgM-1 and IgG-1 allotypes were monitored for several weeks after cell transfer. Donor and host-derived serum allotype concentrations were inversely related, i.e., high donor allotype levels were linked directly to suppression of host allotypes. Donor-derived Ig synthesis in chimeras ceased between 10 and 20 weeks after cell transfer and host allotype levels recovered concurrently. Lymphoid cells from chickens which had rejected donor cells and recovered their host allotype, failed to manifest any suppressive effect on B cells from allotype-matched donors in adoptive transfer experiments. These results agree with our previous conclusion that the mechanism which determines the reciprocal relationship between host and donor allotype synthesis is attributable to a nonimmune surveillance mechanism operating between the respective B cell populations. (B14A x CHA)F1 hybrid recipients were more resistant than MHC-compatible B14A hosts toward the engraftment of B14C B cells. Although chimerism was established in chickens pretreated with cyclophosphamide, it did not occur in sublethally irradiated recipients even when administered in conjunction with antithymus globulin. However, 300 rad abrogated the barriers against T cells, resulting in lethal graft-versus-host (GVH) reactions which failed to occur in untreated recipients. B14C bone marrow cells produced more severe host Ig suppression in F1 hybrid than in B14A recipients. In contrast to the temporary nature of B cell chimerism in histocompatible B14C → B14A pairs, donor-derived allotype levels in Fl hybrid chimeras showed a gradual increase up to 20 weeks after transplantation. We conclude that a mild form of GVH reaction which suppressed the recruitment of host B stem cells prevented the graft rejection and amplified the production of donor-derived immunoglobulins. Hybrid resistance exhibited by Fl hybrid mice against parental haemopoietic cells or tumours is considered to be distinct from classical alloimmune reactions (1). Previous studies have been concerned with genetic control (2), the effector system represented probably by “natural killer” cells (3) and with agents that are capable of abrogating the host barrier (4–6). We have reported recently that juvenile chickens express resistance toward transplanted MHC-compatible B cells and that engraftment in cyclophosphamide (CY)-conditioned recipients resulted in suppression of host-derived Ig synthesis (7). These findings were attributed to a B cell surveillance mechanism similar to that which has been postulated previously to explain the host resistance toward haemopoietic and tumour cells. This paper presents a quantitative and kinetic analysis of donor and host-derived Ig synthesis in B locus (MHC)-compatible and parental → Fl hybrid cell chimeras.