Lack of A/B-antigen equivalent to Rhesus disease Rhesus disease occurs when an Rh- mother is exposed to Rh antigens (often due to blood contact with an Rh+ child during delivery) and mounts an immune response which eventually results in the production of IgG Rh antibodies. In subsequent pregnancies, these antibodies cross the placenta. When the foetus is Rh+, these antibodies can bind to the corresponding antigens on the foetal erythrocytes and cause haemolysis, which can result in anaemia or even, in serious cases, stillbirth. Given all of this, **why does the same principle not apply to A and B antibodies?** In other words, what is special about Rhesus antigens or antibodies that does not apply to other erythrocytic antigens or their corresponding antibodies? I'm specifically wondering about Rhesus disease and its effects on the foetus, and why similar effects do not occur _on the foetus_ in the case of an ABO type mismatch between mother and foetus.

So it turns out it can occur. It's called Hemolytic Disease of the Newborn (ABO), and according to the article (the relevant citations are a book and some journals to which I do not have access), it is very rare, and severe cases are even more rare. Apparently anti-A and anti-B antibodies are typically of the IgM isotype, which cannot cross the placental barrier. However, occasionally IgG is produced, which _can_ cross.

This is what causes the hemolysis in the fetus - if the mother is type O, and the baby is either A or B, the mother is exposed to unknown antigen and produces antibodies. If they happen to class-switch to IgG, they can cross the placenta and, if in large enough quantities, cause the opsonization and lysis of red blood cells.