In this issue of Blood, Jajosky et al demonstrate that passive immunization with red blood cell (RBC) antibodies that have the ability to remove target antigens from RBCs, without affecting RBC clearance or CD4+ T-cell proliferation, can convert an augmented RBC alloimmune response to antibodymediated immunosuppression (AMIS) in an established murine model of RBC alloimmunization. 1 These findings shed light on the mechanisms of AMIS and have the potential to facilitate development of new strategies for AMIS against non-RhD RBC alloantigens to expand the prevention of hemolytic disease of the fetus and newborn (HDFN).

Development of maternal alloantibodies against paternally inherited fetal RBC antigens can lead to HDFN. 2 These maternal antibodies, most commonly anti-RhD, are actively transported across the placenta, where they bind to fetal RBCs carrying the corresponding antigen, which can result in RBC clearance via phagocytic Fcγ receptors (FcγRs). 3 If untreated, this can result in perinatal mortality and morbidity, with the occurrence of fetal anemia, jaundice, hydrops, and stillbirth. 2 Polyclonal anti-RhD immunoprophylaxis administered