Rh factor, ABO incompatibility

[Gospe1]

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So Rh factor fetal-mother incompatibility makes sense. Why doesn't this happen with ABO? The mother can be OO and the baby be AO or BO. The mother would have anti-A and anti-B. Why no erythroblastosis fetalis? Wikipedia says something like most anti-A and anti-B are IgM which can't cross the placenta. Again, why are they igM when anti-Rh are IgG?

 

[clinicallabguy]

The reason is what you said. Anti-A and Anti-B are IgM antibodies, and cannot cross the placenta. They are IgM's because the epitopes they are specific for are carbohydrate moieties. So there is no T-cell help from CD4 cells, because there is no peptide presentation on MHC2. So no class switch.

A antigen: N-acetylgalactosamine
B antigen: Galactose
On a precursor substance.

The ABO blood group system is non-RBC immune, generally speaking. This means that anti-A and anti-B antibodies do not form as a result of a person being immunized with another persons blood. They form naturally, and the way I learned it is we do not know exactly why anti-A and anti-B antibodies form. They may actually be against antigens everyone sees, but cross react with blood group antigens is a hypothesis and negative selection explains why only the antibody specificity a person lacks is formed. But it's like clockwork that they form in everybody. If you're type A then you will have anti-B antibodies. It's amazing that it happens universally.

The Rh system is RBC immune, and is a protein antigen. Protein->Peptide->MHC2->Th->Class switch to IgG. The Rh pos firstborn of an Rh neg mother will likely not develop hemolytic disease of the newborn, but the mother may form IgG anti-D antibodies after the insult with the babies blood. Then subsequent babies will be at risk if they are Rh pos.

 

[MicA]

There are always preformed antibodies in your blood for the ABO system. Hence the immediate rejection of donor blood if it is not suitable. They are IgM. They cannot pass the placenta. I don't think that your body even class switches those antibodies to IgG otherwise it would affect the baby. We actually learnt that the AB antibodies could be due to your body developing something against the intestinal bacteria, though I don't think that people really know because you begin to develop antibodies at around 3 months. I asked this question to a lecturer, the one that you asked, and they mentioned IgM and the fact that sometimes the baby can be born with jaundice, especially if the mother is O and the baby is A or B.

As you know anti-D is an IgG antibody so can pass through the placenta. Make sense because you need to be exposed first to blood at birth before you begin to develop the antibodies.

 

[deuce924]

Just memorize that Anti-A and Anti-B are IgM which can't cross the placenta and Anti-D are IgG which can cross the placenta.

I think the theory behind why ABO are IgM is because the commensal bacteria in your intestine possess these same antigens on the RBC's and are constantly being made to those antigens not found on the body's RBC's thus being IgM.

Also, ABO Mismatch is more commmon than Rh Mismatch but it is rarely symptomatic.

 

[Ariodant]

In most cases the ab will be IgM and blocked by the placenta. However, if the mother is type O, she will develop IgG against A and B, and her second incompatible baby will have hemolytic anemia of the newborn.

 

[Disinence2]

In most cases the ab will be IgM and blocked by the placenta. However, if the mother is type O, she will develop IgG against A and B, and her second incompatible baby will have hemolytic anemia of the newborn.

Anyone Verify this?

 

[Jolie South]

Anyone Verify this?

We just had a lecture on this. ABO HDN exists and is actually becoming more common than Rh HDN (due to Rhogam prevention), but it's not as severe. Hydrops fetalis, kernicterus, and stillbirth are rare.

 

[dru2002]

We just had a lecture on this. ABO HDN exists and is actually becoming more common than Rh HDN (due to Rhogam prevention), but it's not as severe. Hydrops fetalis, kernicterus, and stillbirth are rare.

+1

The majority of cases (65%) of hemolytic disease of the newborn have minor consequences and are caused by ABO blood-group incompatability between the mother and fetus. Type A or B fetuses carried by type O mothers is most likely to develop IgG antibody to the A or B blood-group antigens either through natural exposure or exposure to fetal blood-group A or B antigens in successive pregnancies. Usually the fetal anemia resulting from this incompatability is mild; the major clinical manifestation is a slight elevation of bilirubin, with jaundice. Depending on the severity of the anemia and jaundice, a blood-exchange transfusion may be required in these infants. In general, the reaction is mild, however, and exposure of the infant to low levels of UV light is enough to break down the bilirubin and avoid cerebral damage.

-Kuby Immunology, Sixth edition, pg. 391

It's good to be an immunology major.

 

[Aphtalyfe]

In most cases the ab will be IgM and blocked by the placenta. However, if the mother is type O, she will develop IgG against A and B, and her second incompatible baby will have hemolytic anemia of the newborn.

Anyone Verify this?

We just had a lecture on this. ABO HDN exists and is actually becoming more common than Rh HDN (due to Rhogam prevention), but it's not as severe. Hydrops fetalis, kernicterus, and stillbirth are rare.

Also, other tissues in the fetus, such as vWF, express A or B (depending on the blood type of the fetus) antigens and will effectively soak up some of the IgG that would've bound to the A or B on RBCs. However, Rh is only found on RBCs.

 

[JoshuaR]

As this is VERY related, I felt it more appropriate to respond to this thread than create another. This is merely for my own curiosity.

Why DO Blood Type O mothers produce IgG antibodies against A or B? (we already saw in this thread that these are carbs, not peptides). And also, considering that Type O mothers can produce IgG, why DON'T A or B mothers produce IgG? Why do they only produce, for the most part, IgM?

 

[Leon22]

So Rh factor fetal-mother incompatibility makes sense. Why doesn't this happen with ABO? The mother can be OO and the baby be AO or BO. The mother would have anti-A and anti-B. Why no erythroblastosis fetalis? Wikipedia says something like most anti-A and anti-B are IgM which can't cross the placenta. Again, why are they igM when anti-Rh are IgG?

anti-A anti B IgG do exist in group O individual(dont know how,but it is stated in goljan rr)
but infant of blood group A/B/AB has poor ability of expressing the ABO antigen.
But when it does happen it causes ABO incomptability and causes neonatal jaundice

 

[SpecterGT260]

Anyone Verify this?

If true I see no reason why a A mother couldn't form IgG against B and vice versa