Antigens are polymorphic, inherited, carbohydrate or protein structures on the extracellular surface of red blood cell membrane.
Genes indirectly control the expression of the A, B and O antigens as antigenic activity is determined by sugars liked to either polypeptides or lipids.
Red blood cell types of A, B, and H genes code for a specific glucosyltransferase adding a different sugar on a polypeptide or lipid to form the ABH antigens.
Red blood cell surface antigens are recognized by antibodies made in antigen-negative individuals after exposure to RBC’s through transfusion or pregnancy.
More than 250 antigens in 29 blood groups have been recognized.
ABO system most important of blood type systems and involves three alleles A, B, and O in chromosome a.
The O gene is nonfunctional because it has no detectable blood group antigen.
O blood type gene expression results in loss of production of a functional protein or enzyme.
Type O red blood cells lack A and b antigens, but have abundant H antigen.
H type red blood cells have fucosyltransferase enzyme by adding fucose to terminal galactose and they have H antigens.
Adding N-acetyl-D-galactosamine to the terminal D-galactose of an H antigen by glycosyltransferase will cause red blood cells to have an A antigen on their surface.
If glycosyltransferase adds D-galactose to the H antigen a B antigen results.
ABO specificity is dependent on ABO genes and Hh genes.
Phenotype O associated with genotype OO, antibodies Anti-A, Anti-B with 45% incidence in whites and 49% in blacks.
Phenotype A, A1 or A2, associated with genotype AA or AO, with antigens A1 or A2 and H with anti-B antibodies and 40% incidence in whites and 27% in blacks.
Phenotype B associated with genotype BB or BO with antigens B and H, with antibodies to A and makes up 11% of white and 20% of black blood types.
Phenotype AB with genotype AB and antigens A, B, and H with no antibodies and incidence of 4% in whites and blacks.
Non-O groups have higher levels of von Willebrand factor and factor VIII levels and higher rates of myocardial infarction.
Carbohydrates attached to proteins risk lipids define antigens in the ABO, H and P group systems.
A blood group has two main groups A1 and A2.
A1 blood type has more a antigens sites than A2 blood type cells.
A1 and A2 genes differ by one base pair.
Subgroups of B blood group are rare.
In the ABO system natural occurring antibodies, isoagglutins, are immunoglobulins IgM that activate complement and cause immediate intravascular hemolytic transfusion reactions.
ABO IgM antibodies are absent at birth and develop within 3-6 months of age following exposure to ABH antigens in our environment.
ABO antibodies are developed to ABH antigens that are absent in the individual.
ABO antibodies increase until age of 10 years and subsequently fall with increasing age in adults.
In acquired immunodeficiency states the levels of ABO antibodies may be significantly low.
ABH antigens present in red blood cells and most other tissues of the body and include platelets and leukocytes.
The secretor (Se) gene controls the ability of the patient to secrete soluble ABH antigens.
Approximately 80% of the population has a dominant secretor gene that controls the ability to secrete soluble ABH antigens.
Secretors have soluble ABH substances in plasma and in their saliva, semen and sweat.
Rhesus (Rh) system is the second most important clinical blood group and consists of 50 different antigens.
Lewis and Chido-Rodgers system antigens are acquired by the red blood cell membrane from the plasma.
Antigens of the remaining 24 blood group systems are located on the red blood cell membrane or on glycosylphosphatidylinositol linked proteins.