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ABO system is the most important blood group system that requires a huge consideration in blood transfusion because it can lead to death of the patient and the next most important is the Rh system. The ABO blood group system was discovered in the 1900 by Karl Landsteiner, and he found the A, B, and O and later on in 1902, Decastrello and Sturli discovered the fourth type, AB.
Blood groups are inherited from both parents, The ABO gene is mainly controlled by one gene which is known as the ABO gene, this gene contains three alleles which are the i, IA, and IB. This gene codes for an enzyme that modifies the carbohydrate content of red blood cells antigen which is known as a glycosyltransferase. It is located on chromosome 9q34. Type A blood type arises from the IA allele, and blood types B and O also arise from the IB, i alleles respectively. Due to the dominance of IA and IB, the inheritance trait means that type A and B parents can have an AB child this is known as codominance. A type A and a type B couple can also have a type O child if they are both heterozygous (IBi,IAi) The cis-AB phenotype has a single enzyme that creates both A and B antigens.
There are about twenty subgroups of blood type A, and the most common of this are subgroups A1 and A2, where A1 makes up about 80% of people with blood type A and the rest is made up of A2 individuals. These two subgroups can be interchangeable in transfusion.
In the formation of the ABO blood group antigens, an essential precursor substances is required which forms the H antigen, the H locus is present chromosome 19 where it encodes a fucosyltransferase which is an enzyme that produces the H antigen on the surface of red bloods. The H antigen is made up of a sequence of carbohydrate linked to protein, it is made up of a chain of β-D-galactose, β-D-N-Acetylglucosamine, β-D-galactose, and 2-linked, α-L-fucose which is attached to the protein.
Present on chromosome 9 is the ABO locus which has three main allelic forms which A, B and O. The allele for A codes for an enzyme, glycosyltransferase (N-acetylgalactosaminyltransferase) which causes the bonding of α-N-Acetylgalactosamine to the D-galactose end of H antigen hereby producing the A antigen. The B allele encodes a glycosyltransferase that forms a bond between the α-D-galactose to the D-galactose end of H antigen, creating the B antigen. The O allele has a deletion of a single nucleotide of guanine, this leads to the frameshift leading to formation of a non enzymatic protein hereby means that there is no change to the H antigen, this is the case in group O individuals. (Rudmann, 2005)
Anti-A and Anti-B are formed during the first year of a child growth, there are a lot of hypothesis surrounding how or what causes the formation of this antibodies. They are IgM antibodies except in the case of group individual who can produce IgG antibodies that can cross the placenta both Anti-A and Anti-B cannot cross the placenta so mother and child can have different blood groups and survive well. The table below shows what characteristics each blood group carries thereby affecting how transfusion will be carried out.
Red blood cell type
Anti A and Anti B
A and B antigen
According to the above table it shows that individuals with type A blood can receive blood from donors of type A and type O blood, individuals with type B blood can receive blood from donors of type B blood and type O blood, individuals with type AB blood can receive type A blood, type B blood, type AB blood and type O blood whereas individuals with type O blood can only receive blood from type O blood donors. And this is done in other to avoid complications after transfusion.
The Rh blood group system is the second most important blood group system in transfusion science, it the most polymorphic of all the human blood groups, it is known to consist over 45 independent different antigens which makes it very important in transfusion. Much progress has been made in the research of this particular blood group system because of the recent developments in our ability of making clone complimentary DNA and the genes that code for the Rh proteins which have improved our knowledge about some of the Rh antigens.
Different people over the years have been involved in the nomenclature and naming of the Rh antigen with regards to theories about how they are inherited genetically. There is a numerical system developed by Rosenfield et.al which is recognised by the International Society of Blood Transfusion where the genes that code for the Rh proteins are numbered Rh30 and the Rh glycoproteins are Rh50 with the numbers related to their molecular mass of the proteins on a SDS-polyacrylamide gel. (Turgeon, 1995).
Other nomenclature involves the use of RhD and RhCcEe proteins where they have RhAG for the gene encoding the Rh-associated glycoprotein. The most common Rh antigens are D,C/c, and E/e which were written earlier on in alphabetical order but later changes to DCE when it was realised that C and E antigens are inherited en bloc. The letter d is used to show D negative phenotypes, so there are 8 haplotypes that are coded for by the RHCE and RHD which are Dce, dce, DCe, dCe, DcE, dcE, DCE and dCE which can also be written as R0, r, R1, r', R2, r, Rz, and ry (respectively) where R is used when the D antigen is expressed and r is used when the D antigen is not expressed. There are some deletion phenotypes that use dashes in indicating lack on antithetical antigens such as Dc. RBCs lack E and e antigens, and D RBCs lack C, c, E, and e antigens. RBCs with the Rhnull phenotype do not express any of the Rh antigens.( Cartron, 1994)
The Rh antigens are extremely immunogenic and all the Rh antibodies can cause haemolytic transfusion reaction as well as cause the haemolytic disease of the new born. This is possible because of the difference between the amount of amino acid present on the Rh antigens, D antigen differs C/c and E/e antigens by 35 amino acids this making it very powerful stimulant of an immune response. Most of the antibodies formed against Rh antigens are mainly IgG type which is why they are able to cross the placenta to cause haemolytic disease of the new born as well as haemolytic transfusion reaction, most often the antigens do not activate complement but attach to the red blood cells and cause them to be destroyed by macrophages in the spleen in a process known as extracellular haemolysis. There are few Rh alloantibodies known to occur naturally and are of the IgM type but they are very few in numbers. Rh antigens are only expressed in the presence of the Rh associated glycoproteins.
The D antigen is highly immunogenic and induces an immune response in 80% of D-negative persons when transfused with 200 mL of D-positive blood. For this reason, in most countries D typing is performed routinely on every blood donor and transfusion recipient so that D-negative patients receive D-negative RBC products. On occasions, there have been cases of complications due to mismatched transfusions. In contrast, despite the use of immunosuppressive therapy with anti-D immunoglobulin prophylaxis, D alloimmunization in pregnancy still occurs.
In conclusion, it is essential to regularly do blood testing, to find out all the blood group antigens present in other to avoid complications in blood transfusion.