Following information were obtained by teacher's manual of Carolina Blood Typing (WW-70-0168).  Images and extra information were added to help understanding of materials.

The ABO Blood Group System

The immune system accounts for the variable success of early attempts to transfuse blood. Blood cells from a donor may be destroyed by antibodies in the plasma of a recipient. In the early part of this century, Dr. Carl Landsteiner found four major blood groups (A, B, AB, and O) based on the reactions of donor red blood cells with recipient serum. In this ABO blood group system, there are two antigens, A and B, which may or may not be present on the surface of red blood cells. Two antibodies, anti-A and anti-B, may or may not be present in the blood serum. The ABO blood group system is summarized in Table 1.

Table 1

The ABO Blood Groups

Notice that the serum always contains the antibody for the absent red cell antigen(s). Usually it is necessary for exposure to an antigen to occur before antibodies are produced; however, in this instance the antibodies are already present before any transfusion is attempted. Thus, if we attempt to transfuse group A blood into a group B recipient, the anti-A in the recipient’s blood will cause the A cells to agglutinate. The agglutinated cells will become trapped in capillaries where, after several days, they will rupture and release breakdown products. These breakdown products may clog vital organs such as the kidneys. In extreme cases, the kidneys will fail and death will result.

Obviously, safe transfusions can only occur when the antigenic properties of donor blood are compatible with the recipient’s anti-bodies. Table 1 shows that conditions are safe when both donor and recipient belong to the same ABO blood group. Group AB persons can receive blood from any of the other groups, and group O persons can donate blood to any of the others, although such transfusions are made only in extreme emergencies. The commercial availability of anti-A and anti-B sera (blood sera containing antibodies against the A and B antigens respectively) allows the matching of donor and recipient, an important requirement of the modern blood banking system.

The ABO blood groups are inherited. There appear to be three alleles: I^A, I^B and i.  The genotypes and their corresponding phenotypes (blood groups) are shown in Table 1. Alleles I^A and I^B are dominant to i, but show no dominance with respect to each other. At first it was thought that group O people did not have an antigen.  It is now known that all the ABO blood groups (O included) have H substance, a weak antigen. The presence of the I^A or I^B allele causes the conversion of some H antigen into A or B antigen, respectively.  The i allele produces no change; thus, group O blood generally has more H antigen than does A or B or AB blood.

The production of H antigen is controlled by a gene locus that is independent of the ABO locus. The allele h for the absence of H antigen is rare and the homozygote h/h which produces red cells without H antigen is very rare. This is the Bombay phenotype, named for Bombay, India where it was first discovered. In the absence of H antigen, alleles I_A and I_B are suppressed. When tested with anti-A and anti-B sera, the Bombay phenotype appears to belong to group O; however, group O cells are agglutinated by anti-H, while Bombay cells are not.

Several subgroups of A have been reported. The main division of group A is into subgroups A₁ and A₂.  The other subgroups of A are rare, poorly defined, or questionable. An extract of Dolichos biflorus seed contains a substance which causes a powerful agglutination with A₁ cells but not with A₂ cells. Such substances are known as lectins. The A subgroups are also inherited, the allele for A₁ being dominant to that of A₂.

Although there is variation in the B antigen, the variations are not generally considered significant enough to divide group B into subgroups.

Table 2

ABO Blood Groups

The frequency of ABO blood groups in your class may be compared to the following reported frequencies.

Raw data from Mourant, A. E., Kipec, Ada C., and Domanjewska-Sobezak, Kazimiera, The Distribution of Human Blood Groups, Oxford University Press, London, 1976.

The Rh Blood Group System

Since the discovery of the ABO system, many additional systems have been discovered. The Rh system is the best known of these. The Rh antigen is named for the rhesus monkey in which it was first detected. Today, over 40 human Rh antigens are known; many of them are rare. Obviously, the inheritance of these antigens is complex, and there exist two theoretical models to explain the pattern of inheritance. The Wiener system postulates a single gene locus with a series of at least 10 multiple alleles. The Fisher system assumes the existence of at least three closely linked loci designated C, D, and E. Both systems have advantages and disadvantages and both are currently in use.

Most of the Rh antigens are weak and seldom elicit antibody production; however, the D antigen (Rho in the Wiener system) is a strong antigen and can cause transfusion problems. On the basis of the presence or absence of the D antigen, people can be classified as Rh+ or Rh-. As long as we confine our attention to the inheritance of Rh+ or Rh- blood groups, we can consider this to be a simple case of single gene inheritance with dominance.

The blood serum of an Rh- person does not contain anti-D unless there has been a previous exposure to the D antigen. Thus, the first time an Rh- recipient is transfused with Rh+ blood, little or no effect may be observed because the Rh+ cells are removed from the blood before significant levels of anti-D are produced. A later transfusion of Rh+ blood may produce a dangerous reaction. For this reason, blood banks routinely type blood with anti-D, and only Rh- donors are used for Rh- recipients.

Rh incompatibility between mother and fetus is a major factor in the development of erythroblastosis fetalis or hemolytic disease of the newborn. When an Rh- woman has an Rh+ baby, she can become sensitized to the D antigen. This can seriously affect the health of subsequent Rh+ babies born to the same woman. Normally, blood cells cannot pass across the placenta from the fetus to the mother; however, as the placenta begins to break down (about the time of birth), leakage sometimes occurs. This can allow fetal Rh- cells to enter the mother’s bloodstream. A few days after giving birth, anti-D may appear in the mother’s blood.

During a subsequent pregnancy, an incomplete anti-D is able to pass through the placenta and enter fetal circulation. If this fetus is Rh+, the anti-D will react with its red blood cells, destroying them. This produces fetal anemia. In severe cases, the baby is stillborn. Fortunately, many of these babies can be saved by transfusions, which can even be made before birth.

An understanding of Rh factors has lead to ways of preventing hemolytic disease of the newborn. Tests can reveal the presence of fetal Rh+ cells in the bloodstream of the Rh- mother. When such cells are present, the expectant mother is given injections of anti-D. Because the anti-D reacts with and “covers up” the D antigenic sites on the fetal cells, the mother’s immune system is not stimulated to produce its own anti-D.

Table 3

Rh Blood Groups

The frequency of Rh blood groups in your class may be compared to the following reported frequencies.

Raw data from Mourant, A. E., Kipec, Ada C., and Domaniewska-Sobezak, Kazimiera, The Distribution of Human Blood Groups, Oxford University Press, London, 1976.

The MN Blood Group System

Many other blood group systems have been implicated in cases of transfusion reactions or maternal-fetal incompatibilities. Antisera to the antigen involved are difficult to produce, and the available antisera are primarily needed for medical diagnostic or research use. The MN blood group system is an exception. It is of little medical importance because few people produce anti-M or anti-N even after repeated exposures to the antigens. In this system there are two antigens, M and N. The alleles for production of these antigens show no dominance to each other, so there are three blood groups (phenotypes) with three corresponding genotypes.

Table 4

MN Blood Group System

Since the genotype can in all cases be directly determined from the phenotype, and since all people appear to belong to one of the three groups, this system has been of great interest to geneticists and anthropologists.

In comparison to the genetics of the ABO and Rh systems, the genetics of the MN system may seem wonderfully simple. In reality, the MN system is as complicated as the Rh system. For example, the presence of antigen S is controlled by alleles S and s which are closely linked with the MN locus. A number of rare alleles, such as M^g and M^c are known at the MN locus. A subgroup, M₁ of group M is known. However, if we confine our attention to the main MN groups which are defined by anti-M and anti-N, the system can be viewed as quite simple.

Determining Gene Frequencies

Because the M and N blood groups are determined by a single set of alleles, and because dominance is not involved (making it possible to distinguish the heterozygote MN from both homozygotes MM and NN), many studies of human genetics have used the MN system. Additionally, there does not appear to be any selection pressure against either allele. Thus, the MN system is a good test of the Hardy-Weinberg Law. The differences in frequencies of the M and N alleles between human populations are thought to represent the effects of genetic drift.

Consider the following data. (Remember that each person carries two alleles for MN blood group.)

Gene frequencies can also be calculated from the Hardy-Weinberg law:

Table 5
MN Blood Groups

The gene frequencies for your class may be compared to the following reported frequencies.

Based on data from Mourant, A. E., Kipec, Ada C., and Dornaniewska Sobezak, Kazimiera, The Distribution of Human Blood Groups, Oxford University Press, London, 1976.

Further Reading

Race, R. R. and Sanger, R. 1973. Blood Groups in Man. Blackweli Scientific, Oxford.

Rothwell, Norman V. 1977. Human Genetics. Prentice-Hall, Englewood Cliffs, N.J.

Stine, Gerald J. 1977. Biosocial Genetics, Macmillan, New York.

Watkins, Winifred, M. 1966. Blood-group substances. Science 152: 172—181.