James Chua

 Major blood groups

 ABO
 Rh

 Minor blood groups

 Discovered by Landsteiner, von Descatello and Sturle
 Drew blood from himself and 5 colleagues
 Separated serum from the red cells and mixed them up
 Unknowingly performed the first ever forward and reverse
blood typing
 Red Cells Sera from A Sera from B
person person
(Anti-B) (Anti-A)
O person (No Ag) NEG NEG

A (A Ag) NEG +
B (B Ag) + NEG
AB (A and B Ag's) + +
 Individuals have “naturally occurring” antibodies in
their serum directed against the missing antigens on
the surface of their RBCs
 ABO antibodies are not really “naturally occurring”.
Their production is stimulated by ubiquitous
substances such as:
 Bacteria
 Pollen
 Other substances

 Production of ABO antibodies starts at birth but titers

are too low for detection until 3 to 6 months of age.
 Antibody production peaks at 5 to 10 years but
decreases with age.

 Persons above 65 have low titers for detection.

 IgM
 “Naturally occurring form”
 COLD-reacting
 BIND complement
 DO NOT CROSS placenta
 IgG and IgA
 “Immune forms”
 Results from foreign red cell
stimulation by transfusion or
pregnancy
 General characteristics
 Gycoproteins or glycolipids
 Present in all organs of the body (histoblood group antigens)
 Phenotypic expression affected by several factors:
▪ Age – Develop as early as 37th day of fetal life; Newborn red cells have
only 25 to 50% of the number of antigenic sites found on adult red
cells
▪ Race
▪ Genetic interaction
▪ Disease states
 Inheritance
 Alleles involved: A, B, O, H and Se

 Formation
 Precursor substance: paragloboside
 Addition of sugars
 Formation
 Precursor substance: paragloboside
▪ Red cell surface
▪ Type 2 (terminal galactose and N-acetylglucosamine in beta 1 → 4
linkage) Glycolipid

▪ Body fluids and secretions

▪ Type 1 (terminal galactose and N-acetylglucosamine in beta 1 → 3
linkage) Glycoprotein
 Formation
 Addition of sugars
▪ Glycosyltransferases
▪ Type of glycosyltransferase depends on inherited alleles
Gene Enzyme Nucleotide Sugar Antigen
(Sugar
Donor)
H α-2-L-fucosyl transferase GDP-Fuc L-fucose H

A α-3-N-acetyl- UDP- N-acetyl- A

galactosaminyltransferase GalNAC D-
galactosa
mine
B α-3-D-galactosyl UDP-Gal D- B
transferase galactose
O None None None O
 GDP-Fuc: guanosine-diphosphate L-fucose
 UDP-GalNAC: uridine diphosphate-N-acetyl-D-
galactose
 UDP-Gal: uridine diphosphate galactose
 Secretion
 Secretor status (Sese or SeSe): α-2-L-fucosyl transferase
expression in tissues related to exocrine secretions
 Non-seceretors (sese)
 Fluids in which A, B and H substances can be detected
in secretors
 Saliva, urine, bile, amniotic fluid, tears, digestive juices, milk
and pathologic fluids
 Red cell A, B and H Soluble A, B and
antigens H antigens

Biomolecule Glycolipids Glycoproteins

First sugar Glucose N-acetyl-
galactosamine

Chain Type 2 Type 1

Gene FUT1 FUT2
 Main subgroup (2 schemes)
 A1 and A2
 Aa, Ab, Ac and Ad

 Weak subgroups
 Occur in 1% of the population
 A3, Am, Ax, Ay, Aend and Ael
 First described by von Dungern in 1911
 Quantitative and qualitative differences:
 Concentration of α-3-N-acetyl-galactosaminyltransferase
 Number of antigen sites on red cell
 Antibodies produced
 A1 gene elicits production of high concentrations of α-3-
N-acetyl-galactosaminyltransferase
 Production of 810,000 to 1,170,000 antigen sites
 Presence of A and A1 antigens
 Production of Anti-H cold agglutinin
 Less activity of α-3-N-acetyl-galactosaminyltransferase
than A1
 Production of 240,000 to 290,000 antigen sites
 Presence of only the A antigen
 Production of Anti-A1
 Based on the four different forms of the H antigen
 H antigen forms: H1, H2, H3 and H4
 H1 and H2 are unbranched straight chains
 H3 and H4 are complex branched chains
 H1 and H2 can be converted to Aa and Ab by both A1 and A2
enzymes
 H3 and H4 can only be converted to Ac and Ad by A1 enzyme
and very poorly by A2 enzyme
 So: A1: has Aa, Ab, Ac and Ad
A2: has Aa, Ab, low Ac and no Ad
 Anti-A
 Extracted from sera of type B persons
 Contains both Anti-A and Anti-A1

 Adsorbed Anti-A
 Sera from type B persons are adsorbed with A2 cells
 Contains only Anti-A1

 Dolichos biflorus lectin/ Anti-A1 lectin

 Seed extract that agglutinates A1 cells
 Similar to Anti-A1
 Anti-A (from Adsorbed
B sera) Anti-A/Anti-
A1 lectin
A1 + +

A2 + NEG
 Main subgroup
 α-3-D-galactosyl transferase:
▪ Requires Mn2+ as cofactor
▪ Optimum pH 6.5
▪ Two types: pI's 4.8 to 5.2 and 8.2 to 8.8
 Also based on the four different forms of the H antigen: BI,
BII, BIII and BIV
 Weak subgroups
 B3,Bm, Bx, Bel
 Related to A subgroups
 A1B and A2B
 Lack A, B and H antigens
 Production of anti-H that react at 37°C
 Two types:
 Classical Bombay
▪ hh
 Para-Bombay
▪ Ah, Bh and ABh
▪ Weak expression of A and B
▪ Mutant H (FUT) gene results in low levels of H antigen
 A1 and A1B Anti-H are cold agglutinins
 Bombay Anti-H react strongly at 37°C
 Reactivity: O > A2 > B > A2B > A1 > A1B
 Condition Alteration
Leukemia Weakened A and B antigen
Conditions related to stress expression
hematopoiesis (e.g.,
thalassemia)
Hodgkin's disease

Hypogammaglobulinemia Weakened Anti-A and B

Agammaglobulinemia
Very young and old
populations
 Condition Alteration
Polysaccharides from E. coli Acquired B antigen
(Due to any condition that
increases permeability of
intestinal wall)

Excessive amounts of blood Absence of antigens during

group-specific soluble forward typing; Patients
substances (Due to gastric appear to be blood type O
and pancreatic cancers)
Thank you for your attention.