BLOOD GROUPS

Mansyur Arif
Bag. Patologi Klinik FK UNHAS / RSUP
Dr. Wahidin Sudirohusodo
Definitions
Blood groups are determined by antigens
structures on the surfaces or red cells and
are detected by reactions with specific
antibodies.
A blood group system is defined by
antigens that are regulated either by allelic
genes or closely linked genes.
Table 1. Survey of major Red Cell Blood Group System
System Important antigens
ABO A1,A2,B,H,A3,Am,Ax
MNSs M,N,S,s,U,Mg,Mia,Hu,HeMta,Vw,M2,N2,S2
P P1,pk,P2,(Tja)
Rh D,C,E,c,e,Cw,Ew,ce,Ce,G,CE,cE,Du,Cu,Eu,LW
Lutheran Lua,Lub
Kell K,k,Kpa,Kpb,Jsa,Jsb
Lewis Lea,Leb
Wright Wra,Wrb
Diego Dia,Dib
Cartwright Yta,Ytb
Xg Xga
Dombrock Doa,Dob
Colton Coa,Cob
 Antibodies : sources & properties

1. Normal humans
A.bodies to some blood group a.g occur in
the serum of individuals who lack the a.g
and have had no prior exposure to it
natural isohemagglutinins.
2. Immunized animals

If animals are immunized with human red cells

may form a.bodies to certain of the
xenogeneic blood group a.g important
source of blood group anti sera carefully
absorbed with human red cells to establish
specificity.
Recently developed a.g specific monoclonal
a.bodies do not require such absorption.
3. Immunized humans

The third major source of the blood group anti

bodies are donors who have been allogenically
immunized either by (1) prior blood
transfusions or (2) previous pregnancies
immune antibodies elicited by prior
exposure to red cell a.g are commonly IgGs
 ABO SYSTEM

a. Historical notes
In subsequent work Landsteiner recognized
that the pattern of reactions could be
explained by two a.g, which designated A
and B. O signified the state of not having A
or B.
Table 3. The Landsteiner scheme
Table 3. The ABO system defined by Anti-A and Anti B

Blood Groups Antigens on RC Antibodies in serum

O None Anti-A and Anti-B
A A Anti-B
B B Anti-A
AB A and B None
Genetics
Determining the blood group : genotype and
phenotype. A child receives one of four genes
from each parent : A1, A2, B, or O. Six
phenotypes are possible because the A a.g
associated with group A2 and also A1.
There are ten possible genotypes. Group A1 may
have 3 genotypes (A1 A1, A1 O, A1A2). Group A2
can have either A2A2 or A2 O genotypes. Group
B can have either BB or BO genotypes
 Genotype :
- specific genes that person carries
- determined by family studies
- AA, AO, BB, BO, AB and OO
Phenotype :
Four phenotypes : A, B, AB and O
Although there are ten possible genotypes,
the absence of a specific anti-O prevents the
serological recognition of more than four
phenotypes. (table 5)
 H antigen

The surfaces oligosaccharides that

constitutes the H a.g is the precursor of the
A and B a.g
Gene A & B responsible for converting H
substance into A & B substance
The O gene is an amorph and doesnt
transform the H substance
Rare variant Bombay, the H precursor
cannot be converted to H lack H ag &
hence A or B phenotype cant be expressed.
A terminal sugar molecules determine a.g
specificity :
A a.g : N acetylgalactosamine
B a.g : galactosa
Rhesus System
Rhesus a.b >> immune (previous
transfusion or pregnancy), naturally <<
Anti-D is responsible for most of the clinical
problems associated with the system the
simple subdivision of subjects into Rh D +
and Rh D , using anti-D is sufficient for
routine clinical purposes.
A. Nomenclature : relation to genetic models

1. Fischer-Race theory (table 6) :

Postulates 3 closely linked genes Cc,
Dd and Ee. Rhesus a.g is renamed D.
Rhesus positive presence of the D
antigen, also called Rh or Rh factor
Rhesus negative absence of D but
doesnt denote absence of other a.g
of the Rh system (C,c,E or e)
 2. Weiner system
3. Rosenfield system
B. Compound antigens
C. Weakened antigens :
- weakly reactive ag Du
- formal terminology : Rh +, Du variant
- for transfusion : Du is equivalent to Rh +
D. Deleted antigens : Rh null cells.
E. Rh antigens structure
Table 6. Rh gene complexes

Fischer-Race Wiener
CDe R1
cde r
cDE R2
cDe Ro
CwDe R1W
cdE ru
Cde r1
CDE Rz
 Other clinically significant systems

1. Kell system
The Kell a.g system rivals the Rh system in its
complexity and clinical importance. Appearing in
response to prior immunization, anti-Kell a.b have
caused hemolytic transfusion reactions and HDN.
The main a.g pairs : K-k, Kpa-Kpb and Jsa-Jsb
2. Duffy system
Double negative phenotype red cells, Fy (a-b-) are
totally resistant to invasion by Plasmodium vivax.
Transfusion of incompatible blood into Duffy-
sensitive individuals can cause severe hemolysis.
3. Kidd system
Immunization to Kidd is caused mainly by
transfusions. Kidd a.b are evanescent warm-active
incomplete a.b that may not be detected in red cell
a.b screens. Consequently they often cause
delayed transfusions rx, which may be severe.
4. Lutheran system
There are 2 common alleles, Lua and Lub and a
silent one. The double-negative phenotype caused
by either dominant inhibitor gene or a recessive
silent allele.
5. Xga blood group

This a.g is controlled by a gene on the X

chromosome. Its not clinically significant but
is of interest as a marker for X chromosome
that appear to escape inactivation by the
Lyon mechanism.
The ABO and Rhesus (Rh) groups are of major clinical
significance. Some other systems of less overall importance
are listed in table 7.
Systems Frequency of a.body Cause of HDN
ABO Very common Yes
Rh Common Yes
Kell Occasional Yes
Duffy Occasional Yes
Kidd Occasional Yes
Lutheran Rare No
Lewis Occasional No
P Occasional Yes (rare)
MN Rare Yes (rare)
Ii Rare No
 Uses of blood grouping data

A. In clinical medicine
1. Pretransfusion testing :
Prior to transfusion, blood is typed
and crossmatched to establish ABO and
D compatibility
2. Hemolytic disease of the newborn
B. In genetics chromosome mapping
C. In forensic medicine :
1. Identification studies
2. Paternity testing