BLOOD BANKING

ABO Blood Group

BT Father
 Clinical Significance: HTR’s or HDN’s A B AB O

Mother
 Most Significant Antibody: “Warm Reactive” (37° or Indirect A A, O A, B, AB, O A, B, AB A, O
Antiglobulin Test) B A, B, AB, O B, O A, B, AB B, O
 Most Insignificant Antibody: “Cold Reactive” (below 37°; may AB A, AB, B A, B, AB A, B, AB A, B
react during in-vitro test, blood typing, crossmatching, and O A, O B, O A, B O
other serologic test.)
ABO Antigens: Biochemical and Genetic Consideration
 Warm Antibodies are mostly IgG (can pass placenta making it
possible to cause HDN), while Cold Antibodies are usually IgM.
 IgM Antibodies are usually “naturally occurring” (no transfusion
or pregnancy required for their formation)
 ABO Blood Group System is primarily consisting of IgM
antibodies.
 Rh Blood Group System is primarily consisting of IgG antibodies.

Proteolytic Enzymes

Enhanced Decreased Unaffected

1. ABO related 1. MNS System 1. Kell System
-ABO/H Systems 2. Duffy System 2. Diego System
-Lewis Systems 3. Lutheran 3. Colton System
-I Systems System
-P Systems
2. Rh System *don’s make use of
3. Kidd System enzymes because
eventually this will
destroy the
components of
these systems
 Lewis System:
- not organically in the RBC antigens
- a soluble antigen found in the plasma
- only is absorbed in the RBC wall
History

 Karl Landsteiner
- 1901: ABO Blood Group System discovery
- Landsteiner and 5 coworkers began mixing each other’s RBC
and serum, and inadvertently performed the 1st forward and
reverse ABO grouping.
- ISBT Number -001

Why is ABO important?

 ABO compatibility: Donor’s RBC (antigen) + Patient’s serum

(antibody)
- Essential foundation of pre-transfusion testing
 Only system with expected antibodies (Rh antibodies– immune
induced antibodies)
 Whether IgG or IgM, ABO can activate complement leading to
HTR
*Rh antibodies – regardless if you’re Rh (-) or Rh (+), you don’t have
anti-D. It will only be produced when you’re introduced with Rh(+)
 Precursor Substance
blood transfused to Rh (-) blood.
- May be present in the ABO
- May emanate in the wall of the RBC, plasma, or body
secretions. (Glucose, Galactose, N-acetylglucosamine,
Galactose -polysaccharides)

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 Type 1 - found in secretions (glycoproteins) and plasma O A B AB

(glycolipid), ß1-3 linkage A1 A1 Anti- 4+ 0 4+ 0 4+ 0
 Type 2 – found in RBC wall/membrane (glycolipid/glycoprotein), B
ß1-4 linkage A2 A2 Anti- 4+ 0 4+ 4+ 4+ 0
B,A1
Features H Gene ABO Gene Secretor B B Anti- 0 4+ 4+ 4+ 0 0
Gene A
Chr LOCI Chr 19q13 Chr 9q34.1 Chr 19 AB A,B - 4+ 4+ 4+ 0 0 0
Alleles H and h A, B, and O Se and se O H Anti- 0 0 0 4+ 4+ 0
alleles (h is alleles (O is alleles (se is A,B
amorph) amorph) amorph) Oh - Anti- 0 0 0 4+ 4+ 4+
Genotypes HH AA/AO SeSe(secretor) A,B,H
Hh BB/BO Sese(secretor)
hh OO sese(non-  Type A – mostly are Type A1 (80%)
AB secretor)
 Dolichos biflorus lectin – has properties of anti-A1 lectin
Phenotypes H A Se Bombay OH BGS
(can be done H (Bombay) B se  ISBT Number – 018
by typing O
 Discovered by Bhende et al (1952)
using anti- AB
 Found in Bombay (Mumbai)
sera)
 Very rare (130 worldwide)
Enzyme FUT1 NAGT (A) FUT2
 Due to recessive gene at H-locus – h as Oh
DGT (B)
 Mutation at position 316 from a tyrosine to a stop codon – Oh
Sugar L FUCOSE NAG L FUCOSE
phenotype
DG
 Bombay Oh – highest anti-H
Bombay phenotype
 H, ABO, and Secretor Genes are interrelated.
 “Para-Bombays” – secretor
- H Gene – dictates or change the precursor substance into an
- Intermediate form of H-gene
antigen, H-antigen.
 Para-Bombay phenotype
- H-antigen – once present, can dictate the RBC antigen/ABO
- Similar to Bombay but have Se to partially compensate for
antigens that may be present in the RBC wall, secretions, and
lack of H.
plasma. (ABO)
- Phenotype: Ah, Bh, ABh
 FUT1
- RBCs may type like Bombay’s, but serum testing shows H & A
- Will catalyze polysaccharide in RBC wall
or B Antigen (unless Group O)
- Will attach to L Fucose in precursor substance and will
- Have anti-H in serum
convert precursor substance to H-antigen
 FUT2 ABO BGS
- Responsible to convert precursor substance in secretions and
 Relationship is reciprocal
plasma by attaching to L Fucose to become H-antigen.
 More A or B is made, less H remains
 H-antigen
 Relative amounts of H by blood group
- Great-Least: O>A2>B>A2B>A1>A1B
 O>A2>B>A2B>A1>A1B
- Highest H-antigen = O
- Highest Anti-H = A1B
ABO Testing
- Anti-H Lectin – Ulex europaeus
Cell Typing Serum Typing
Blood Genotype ABO RBC Serum  Forward grouping  Reverse grouping
type Enzymes Antigens Antibodies  Patient’s RBCs agglutinated  Back typing
“A” AA, Ai “H”, “A” H, A Anti-B by known sera (anti-A, anti-  Patient’s serum/plasma vs
B) A1 % B RBCs
“B” BB, Bi “H”, “B” H, B Anti-A
 More reliable – antigen is
“AB” AB “H”, “A”, H, A, B none more stable
“B”
“O” Ii “H” H Anti-A, NOTE THE OPPOSITE REACTIONS
Anti-B  If forward reactions is not opposite of reverse, ABO discrepancy
is present.
 Both serum and cell typing are required unless testing babies <4
months of age or reconfirming testing done elsewhere (cell
typing only).
AB Ag Ab Anti- Anti- Anti- A B O

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ABO BGS: ABO Antigen and Antibody A subgroups

Antigens Antibodies  A1 (80%) and A2 (20%)
Based on combinations of 3 Clinically significant and  A1 RBCs 4x more A Antigen than A2 cells
genes on Chr 9: A, B, O “naturally occurring”  Qualitative difference also exist in interactions and shapes of
the Antigens
ABO Antigens are not restricted to RBC membrane  Small % of A2s 91-2% of A2 and 25% of A2B) form anti-A1
 All body fluids except spinal fluid if the individual has inherited (usually clinically insignificant nut can cause discrepancies in
a secretor gene ABO testing)
 Most epithelial and endothelial cells  Lectin of Dolichos biflorus agglutinates A2 RBCs, to differentiate
 Lymphocytes and platelets adsorbed from plasma (have an A1 from A2.
adsorbed form of A and B antigen)
A1 and A2 subgroups
Anti-A Anti-A1 Anti-H ABO ab # of
Group O
antisera antisera antisera in antigen
 Antigen: H serum sites
 Generally, most common blood group per RBC
 Genotype: OO A1 4+ 4+ 0 Anti-B 900x103
 Antibodies: Anti-A, Anti-B, Anti-A,B A2 4+ 0 3+ Anti- 250x103
 Characteristically, very strong B&A
 Mostly IgG, so they cross the placenta to cause mild HDFN
 IgM can’t cause HDN primarily because it can’t cross placenta
 Lectin of Ulex europaeus agglutinates cells with abundant H Other A subgroups
antigen  There are other additional subgroups of A
- AINT (intermediate), A3, AX1, Am, Ael, Abantu
Lectin Specificity  A3 red cells cause mixed field agglutination when polyclonal
 Dolichos biflorus - A2, Sd2 anti-A or anti-A,B is used
 Ulex europaeus - H  Mixed field agglutination appears as small agglutinates with a
 Vicea graminea - N background of unagglutinated RBCs
 They may contain anti-A1

Group B
 Antigen: B, H
 Genotypes: BB, BO
 Antibodies: Anti-A (primarily IgM)
 B subgroups:
- Unimportant and less frequent
- Mixed fields

B subgroups
 B subgroups occur less than A subgroups
 B subgroups are differentiated by the type of reaction with
anti-B, anti-A,B, and anti-H
 B3, Bx, Bm, and Bel

ABO subgroups
 Weakened or variant expression of A and/or B attributes to
inheritance of variant forms of transferases
Group A  Individuals that have neither transferases, inheritors of 2
amorph genes, are group O
 Antigen: A, H  To date, 14 A alleles, 14 B alleles and 8 O identified at
 Genotype: AA, AO molecular level
 Antibodies: Anti-B (primarily IgM)

Lectin Specificity
 Dolichos biflorus - A1, Sd2
 Ulex europaeus - H
Group ABO
 Vicea graminea - N
 Least frequent (4%)

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 Antigens: A , B (very little H)

 Further subdivided into A1B or A2B depending on status of
the A antigen
 Antibodies: none

A, B, H Ag changes associated with disease states

 20-30% of with acute leukemia → depression of A, B, or H
antigens
 AML – Serum H – transferase level reduced
 CML – Serum H – transferase level increased

Other features

 Alterations of ABH expression found in various forms of CA

 ABO Antigens may play a role in resistance to bacteria or
viruses
 Other traits associated with genes in Chr 9
- Galactosemia
- Nail-patella syndrome
- Xeroderma pigmentosa