BLOOD

GROUPS
Why is it IMPORTANT

to know

our Blood group ????

 On basis of blood groups, human beings can be
divided into several categories.

 If blood from one category transfused to another

category without knowing blood groups of
Recipient and Donor, MISMATCHING may
occur which may lead to hazards complications,
even death.
 BASIC TERMINOLOGY
 Agglutinogens:  Agglutinins:

- Antigen - Antibodies against the

agglutinogens
- present on red cell membrane
and body tissues n Body - present in the plasma
fluids.
- plasma Immunoglobulins
- Chemically glycoproteins or
glycolipids
IMP…..

 Antibodies are developed only when body

is challenged by an antigen

 Antigenic stimulus leads to antibody

production by Immune system.
 Agglutination:
-Antigen-Antibody reaction caused by antigen
present on red cell membrane in the presence of
corresponding Antibody in plasma

Agglutinogen Corresponding
( antigen ) Agglutinin
( antibody )
A Anti-A ( alpha )
B Anti-B ( beta )
 For each type of agglutinogen (antigen– Ag ), there is
specific agglutinin (antibody- Ab ) which alone will
produce antigen-antibody reaction

 IMMUNOLOGICAL REACTION
Blood group systems
 Large number of such antigens have been
discovered till now

 According to that there are different blood

group systems

 Till now there is knowledge of 30 systems of

blood groups
History
KARL LANDSTEINER

 Discovered the
ABO Blood Group
System in 1901
 LANDSTEINER LAW

If an agglutinogen present on red cell membrane,

the corresponding antibody must be absent in the
plasma

If an agglutinogen absent on red cell membrane, the

corresponding antibody must be present in the
plasma
PHYSIOLOGICAL BASIS
OF
BLOOD GROUPS
 ABO
SYSTEM
 The blood group We belong to depends on what we have
inherited from our parents.
(Genetic Basis)

 Blood group is determined on the basis of presence of

antigen on surface of RBC

 Two antigen A and B

 there are four different kinds of blood types:

A, B, AB or O (null).
 A & B AGGLUTINOGENS
 Sites of agglutinogens Besides RBCs:
Body tissues - salivary glands, pancreas, kidney,
liver,testis.
Body fluids - saliva, amniotic fluid, & semen.

 The antigens on the red cell membrane are

glycolipids,
while in the tissues & body fluids are glycoproteins.

 They first appear in the sixth week of fetal life

 ANTI-A & ANTI-B AGGLUTININS
 Alfa & beta agglutinins are IgM types

 They can’t cross placenta

 They act best at low temperature (5°-20° C)

Cold antibodies

 They are absent at birth, appear 10-15 days after

birth, reaching maximum at 10 years.
IMP…..

 Antibodies are developed only when body is challenged

by an antigen

 Antigenic stimulus leads to antibody production

WHY IS THIS ?????
 Antigens very similar to the A & B antigens are also
present in the intestinal bacteria, food such as plants,
seeds, and in House dust

so when newborn is exposed to these antigen, these are

absorbed into the blood & stimulates formation of
antibodies against those antigens recognized as “Non-
Self” by immune system

 Anti-A and Anti-B is produced.

What happens to Anti-A and Anti-B ???

Antibody remaining
Blood Group Antigen
( in Plasma )

A A Anti-B

B B Anti-A

AB A&B Nil

O NIL Anti-A & Anti-B

 H ANTIGEN
 Basic Ag present in all individuals

 Has no Antigenic activity.

 A and B Ag are built upon H Ag.

How???
H antigen
RBC

Glucose

Galactose

N-acetylglucosamine

Galactose

Fucose
A ANTIGEN

RBC

Glucose

N-acetylgalactosaminyl Galactose
transferase
N-acetylglucosamine

Galactose

Fucose N-acetylgalactosamine
 B ANTIGEN

RBC

Glucose

Galactose
D-galactosyltransferase
N-acetylglucosamine

Galactose

Fucose Galactose
 Rh
SYSTEM
HISTORY
 discovered by
Landsteiner and
Weiner in 1940
after work on Rhesus
Monkey.
 Scientists sometimes study Rhesus monkeys to learn
more about the human anatomy because there are
certain similarities between the two species.

 While studying Rhesus monkeys, a certain blood

protein was discovered. This protein is also present in
the blood of some people. Other people, however, do
not have the protein.

 Rh (for Rhesus) Antigen or factor.

 Rh positive (Rh+).
 Rh negative (Rh-).
RH ANTIGENS

 There are three antigen C , D , and E

 Important one is antigen D as it produce lethal

transfusion reaction

 Rh positive & Rh negative ( Rh +ve and Rh –ve)

 They can’t be detected in Body tissues & body fluid like

A & B antigen.
RH ANTIBODIES
 No naturally occurring antibody in Rh system
 Antibodies develop only when body is exposed to
Rh antigen.

Blood group Antigen Antibody

Rh positive D Nil

Rh negative Absence of D Nil

 Rh antibodies are produced only when Rh –ve individual is
transfused with Rh +ve blood

 Rh –ve mother gives birth to Rh +ve baby

Once produced, the Rh antibodies persist for years &
produce serious reactions during 2nd transfusion
 These antibodies are Ig G type

 They can easily crosses placenta

 They react best at body temperature . Hence called

warm antibodies
Erythroblastosis foetalis

OR

Hemolytic disease of the newborn

 Mother is Rh negative and fetus is Rh positive

 Fetus having antigen (D) While mother lack this antigen

 For mother this antigen is foreign particle and would

give immune response
Normally fetal RBC do not contact with maternal blood

Butduring child birth, following some trauma fetal RBC

come in contact with maternal blood

Once fetal RBC (containing D antigen) come in maternal

circulation (mother is Rh negative), antibodies production
starts in maternal circulation
Now during second pregnancy

If fetus is Rh positive (presence of D antigen)

Rh antibodies from maternal blood cross placenta to enter

fetal circulation (this antibodies of Ig G variety and can
cross placenta)

Hemolysis of fetal RBC

 Ultimate outcome depends on degree of hemolysis.

 in severe condition, Haemolytic anaemia develops.

 Fetal body tries to compensate as a result large
number of premature erythrocytes ( erythroblast ) is
seen in peripheral circulation of fetus.

 Hence name is Erythroblastosis foetalis

CONDITIONS

 Mother is Rh negative
 First fetus is Rh positive
 Second fetus is Rh positive
 No harm to mother (as far as pregnancy is concern)
 Problems to second fetus
Is it possible that first fetus would
suffer erythroblastosis foetalis

?????
 Yes
 If mother has received Rh positive blood
transfusion before first fetus.
 CLINICAL FEATURES

1) Erythroblastosis fetalis:
- Large numbers of erythroblasts
- Excessive hemolysis of RBCs by Rh antibodies
- Infant may die of severe anaemia.

2) Icterus gravis neonatorum:

- Jaundice due to excessive destruction of RBCs
- Hepatomagaly
3) Kernicterus:
- Bilirubin crosses BBB & deposited in basal ganglia
- Occurs when bilirubin level > 18 mg/dl

4) Hydrops fetalis:
- Grossly oedematous
- Intrautrine death or
if born prematurely or even at term, infant dies within
few hours.
 PREVENTION & TREATMENT
Prevention:
- By injecting single dose of Rh antibodies in the form of
Rh Ig to the mother soon after the 1st delivery.
- These antibodies will destroy Rh +ve RBCs of the fetus
which enters in maternal circulation
- So active antibodies will not be formed by mother

Treatment:
- Replacement of baby’s Rh +ve blood with Rh –ve
blood
Exchange transfusion
Why is Rh incompatibility so
dangerous when ABO incompatibility is
not during pregnancy ????
• Most anti-A or anti-B antibodies are of the IgM class
(large molecules) and these do not cross the placenta.
Thanks
 ABO blood group system

Antigen Antibody
Blood Group
( on surface of RBC) ( in Plasma )

A A Anti-B

B B Anti-A

AB A&B Nil

O NIL Anti-A & Anti-B