Haemolytic disease of the newborn (HDN) is a condition in which the lifespan of the fetal/neonatal red cells is shortened due to maternal alloantibodies against red cell antigens inherited from the father. Maternal IgG can cross the placenta, thus IgG red cell alloantibodies can gain access to the fetus. If the fetal red cells contain the corresponding antigen then binding of antibody to red cells will occur. When the antibody is of clinical significance (e.g. anti-D, -c, -E, -K, -Jka), and of sufficient potency, the coated cells will be prematurely removed by the fetal mononuclear phagocytic system. The effects on the fetus/newborn infant may vary according to the characteristics of the maternal alloantibody. The antibodies giving rise to HDN most commonly belong to the Rh or ABO blood group systems. The morbidity of Rh HDN is explained by the great immunogenicity of the D antigen; HDN due to anti-c is also important and its incidence comes second amongst the cases of severe HDN closely followed by the non-Rh antibody, anti-K. (The anaemia caused by anti-K is more properly called alloimmune anaemia of the fetus and newborn as it is due to direct inhibition of erythropoiesis by the antibody and haemolysis is not a feature.) Antibodies against antigens in almost all the blood group systems (e.g. Duffy, Kidd, etc.) and against the so-called ‘public’ and ‘private’ antigens, have also been responsible for HDN. However, IgM cannot cross the placenta and Lewis and P1 antibodies, which occur frequently during pregnancy, are usually IgM and do not lead to HDN. Furthermore, the Lewis antigens are not fully developed at bir