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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
MNSs
P
Rh
Lutheran
Kell
Lewis
Wright
Diego
Cartwright
Xg
Dombrock
Colton

A1,A2,B,H,A3,Am,Ax
M,N,S,s,U,Mg,Mia,Hu,HeMta,Vw,M2,N2,S2
P1,pk,P2,(Tja)
D,C,E,c,e,Cw,Ew,ce,Ce,G,CE,cE,Du,Cu,Eu,LW
Lua,Lub
K,k,Kpa,Kpb,Jsa,Jsb
Lea,Leb
Wra,Wrb
Dia,Dib
Yta,Ytb
Xga
Doa,Dob
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
A
B
AB

None
A
B
A and B

Anti-A and Anti-B


Anti-B
Anti-A
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)

B.
C.

D.
E.

2. Weiner system
3. Rosenfield system
Compound antigens
Weakened antigens :
- weakly reactive ag Du
- formal terminology : Rh +, Du variant
- for transfusion : Du is equivalent to Rh +
Deleted antigens : Rh null cells.
Rh antigens structure

Table 6. Rh gene complexes


Fischer-Race
CDe
cde
cDE
cDe
CwDe
cdE
Cde
CDE

Wiener
R1
r
R2
Ro
R1W
ru
r1
Rz

Other clinically significant systems


1.

2.

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
Duffy system
Double negative phenotype red cells, Fy (a-b-) are
totally resistant to invasion by Plasmodium vivax.
Transfusion of incompatible blood into Duffysensitive 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

ABO
Very common
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

Yes

Cause of HDN

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

terimakasih

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