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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.

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  • $\begingroup$ It does happen. That's why you need to know a patient's blood type before giving a transfusion - AB is the universal acceptor, and O is the universal donor. $\endgroup$ – MattDMo Aug 3 '15 at 7:04
  • $\begingroup$ This question is specifically about the effect on the foetus in pregnancy, not normal blood agglutination. Sorry for the confusion; I'll edit the question to clarify. $\endgroup$ – Watercleave Aug 3 '15 at 7:15
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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.

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    $\begingroup$ It occurs much less commonly for a reason. Many/most people who produce natural antibodies against the A and B antigens they do not possess. (Type Os against both A/B, As against B, etc). These antibodies are typically IgM produced by a specialized class of B cell (B-1 B cells) independent of a T-cell response. The coating of fetal RBCs with these IgM antibodies in the maternal blood stream facilitates their removal while dampening the generation of a T cell response against these antigens. B-1 B cells may also be resistant to IgG class switching. $\endgroup$ – InactionPotential Aug 3 '15 at 16:57
  • $\begingroup$ One more point is that the ABO antibodies are cold antibodies. They react when the temperature is less than the body temperature generally. $\endgroup$ – One Face Aug 5 '15 at 16:50
  • $\begingroup$ @OneFace do you have citations for that? I honestly don't believe a word of it. Why would the human body make antibodies that bind optimally below 37°C? It's not doing Western blots... $\endgroup$ – MattDMo Aug 5 '15 at 21:07
  • $\begingroup$ webmd.com/a-to-z-guides/cold-agglutinins MattDMo, it is good practice to check if something is wrong before accusing! $\endgroup$ – One Face Aug 6 '15 at 1:14

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