Blood Group Antigens

The History Behind The Blood Group of Humans

In 1901 Karl Landsteiner demonstrated the existence of blood group antigens on human red blood cells as well as antibodies directed against those antigens in human sera. Blood was collected from members of his laboratory staff. He then separated the red blood cells from the serum, and then studied the results of mixing serum and red blood cells from different individuals. He discovered that some sera could agglutinated the red blood cells of some individuals but not others. He realized that individuals could be grouped. Group A individuals had an antigen, called A, on their red blood cells and antibodies to another antigen, called B, in their serum. Group B individuals had antigen B on their red blood cells and antibodies to antigen A in their sera. A third group, called group O, had neither A nor B on their red blood cells but had both anti-A and anti-B in thier sera. Some time later, individuals were described who had both A and B antigens on their red blood cells but no antibodies to A or B in their sera. This group was called AB.

Table 1. ABO blood group. ABO genotypes and corresponding phenotypes, agglutinations, and isohemagglutinins.

Genotype	Blood group phenotype	Antigens on erythorcytes	Serum antibodies
AA or AO	A	A	Anti-B
BB or BO	B	B	Anti-A
AB	AB	A and B	None
OO	O	None	Anti-A and Anti-B

Figure 1. ABO blood group. Structure of terminal sugars, which constitute the distinguishing epitopes, in the A, B, and O blood antigens.

Paternity Exclusion Testing

Figure 2. Knowing the blood types of the mother, the baby, and the supected father(s), the probability of paternity can be determined. This testing can only determine that someone is not the father or that he might be the father.

Rhesus System

In 1940 Landsteiner and Wiener showed that antibodies produced against the rhesus monkey red blood cells agglutinated the red blood cells of 85% of a human population. The antibodies were directed against a molecule called the rhesus (Rh) antigen, and individuals possessing it were called Rh positive. The remaining 15% who did not carry it were called Rh negative. Natural antibodies against the Rh antigens do not occur. Rhesus antigens are unique nonglycosylated, very hydrophobic cell surface proteins of 32 kDa. They are structurally related to the band 3 and band 4.5 glycoproteins, which suggests that they too may be transporter proteins (fig.30.3)

Rh Incompatability

Hemolytic disease of the newborn (HDN) often occurs as a result of rhesus incompatibility. It occurs when an Rh-negative mother carries an Rh-positive fetus. The fetal red blood cells are separated from the mother's circulation by the layer of cells in the placenta called the trophoblast. However, during late pregnancy, and especially during the process of childbirth, the fetal red blood cells may escape into the mother's circulation. Once these cells reach the mother's circulation, they are perceived as foreign and therefore provoke an antibody response. (fig.13.8)

Antibodies to fetal red blood cells are not usually made before first childbirth. Repeated pregnancies provoke high antibody levels in the mother. Maternal IgG antibodies provoked in this way can cross the placenta and reach the fetal circulation, where they react with the fetal red blood cells and cause their destruction and eventually death.

Prevention

HDN does not develop if the parents have differing ABO blood groups. This is because any fetal red blood cells entering the mother's circulation in these ABO-incompatible individuals are immediately destroyed by preexisting antibodies and therefore will not provoke an immune response. These natural antibodies rarely cause hemolytic disease themselves since they are of the IgM class and thus cannot cross the placenta to reach the fetus.
Due to this observation, it was predicted that, if the mother had preexisting anti-Rh antibodies, these would destroy any Rh-positive red blood cells entering the maternal circulation and prevent sensitization.

Figure 5. Passively administered anti-D serum ( produced in males) is given to the mother within 72 hours of any delivery at which she might be sensitized. Her sensitization is effectively prevented.

Return

This page is maintained by the Natural Toxins Research Center at Texas A&M University - Kingsville.