Essay on the Development of Blood Group Antigens and Antibodies

Development of blood group antigens begins in the sixth week of fetal life. Their concentration gradually increases and at the time of birth their quantity reaches to one fourth of the adult level. The adult level is reached at about puberty.

Natural anti A and anti B antibodies are IgM type and their development takes place during childhood from exposure to colon bacteria that normally inhabits the lower gastro intestinal tract.

Since the antigens of colon bacteria are similar to the blood group antigens, the antibodies developed against the colon bacteria cross react with the antigens of foreign red blood cells. Immune systems tolerance to self antigens prevents development of antibodies against the antigens present on their own RBC.

Absence of antibodies in AB blood group and presence of anti A and anti B antibodies in O blood group indicates the tolerant nature of immune system to their self antigens.

Time of Appearance

Anti-A and anti-B production generally begins after the first few months of life. Occasionally infants can be found with already produced antibodies at the time of birth.

Antibody production remains fairly constant until late in adult life. In elderly people, anti-A and anti-B levels may be lower than those seen in young adults.

Since antibody production normally begins after birth, results that are obtained with the sera of newborns or infants of about 4-6 months of age cannot be considered valid because, the antibodies may have been acquired through the placental transfer from mother.

Reactivity of Anti-A and Anti-B

Anti-A and anti-B antibodies are usually IgM and do not pass through the placenta, but some mothers “naturally” have IgG anti-A or IgG anti-B antibodies, which can pass through the placenta.

Maternal IgG antibodies with specificity for the ABO blood group system when passed through the placenta to the fetal circulation can cause hemolytic of fetal red blood cells, leading to fetal anemia and ABO hemolytic disease of the newborn.

Although very uncommon, cases of ABO hemolytic disease of the newborn (also known as ABO HDN) have been reported in infants born to mothers with blood groups A and B.

Some mothers may be sensitized by fetal-maternal transfusion of ABO incompatible red blood and produce immune IgG antibodies against the antigen they do not have and their baby does.

For example, when a mother of genotype OO (blood group O) carries a fetus of genotype AO (blood group A) she may produce IgG anti-A antibodies. The father will either have blood group A, with genotype AA or AO, or more rarely, have blood group AB, with genotype AB.

Almost always, blood group of an individual is constant for life time, but very rarely an individual’s blood type changes through addition or suppression of an antigen by infection, malignancy, or autoimmune disease.

An example of this rare phenomenon is the case of Demi-Lee Brennan, an Australian citizen, whose blood group changed after a liver transplant.

Another more common cause in blood-type change is a bone-marrow transplant. Bone- marrow transplants are performed for many having leukemia and lymphoma, among other diseases. If a person receives bone marrow from someone who is of a different ABO type (e.g., if type A patient receives a type O bone marrow), the patient’s blood type will eventually convert to the donor’s type.

Some blood types are associated with inheritance of certain diseases; for example, the Kell antigen is sometimes associated with McLeod syndrome.

Certain blood types may affect susceptibility to infections, for example resistance to specific malaria species is seen in individuals lacking the Duffy antigen.

The Duffy antigen, presumably a result of natural selection, is less common in ethnic groups from areas with a high incidence of malaria.