The Pathogenesis of ABO Haemolytic Disease of the Newborn

Summary. A study of the pathogenesis of ABO HD is essentially a study of the interrelationships of the maternal IgG anti‐A/anti‐B antibodies with the various components of the ‘protective mechanism’. There is an equilibrium of IgG antibodies across the placenta and thus, ABO HD occurs more frequently in cases with high titre IgG antibodies than in cases with low titre IgG antibodies. The foetal blood group substance ‘protects’ the infants by competing with the red cells for the incompatible antibodies. Small amounts of the homologous blood group substance reduce the IgG anti‐A/anti‐B reaction with A/B red cells and the degree of inhibition increases as the antigenic strength of the red cells decreases. Possible reasons for the difference in combining power of the various adult and foetal red cells are discussed. A small deficiency of non‐secretor infants and fathers was observed and the possible roles of secretor status in ABO HD are discussed.