Other Blood Group System (GROUP MEMBERS: (FATIN NUR AZIRA BINTI AZHARI…
Other Blood Group System
Duffy Blood Group
Encoded by the FY gene with two main alleles, FYA and FYB (codominant)
A receptor for Plasmodium vivax, parasite that invades RBC and causes malaria
(Without Duffy receptor, no malaria)
A receptor for chemicals that are secreted by blood cells during inflammation
Number of antigens: 6: Fya, Fyb, Fy3, Fy4, Fy5, Fy6
Antibody: mainly IgG (IgM is rare)
Discovered in 1950, named according to a patient.
Bombay Blood Group
Found in 1 of 10,000 in India & 1 in a million in Europe.
H antigen deficient, caused by mutation [Genotype: (h/h)].
Have antibodies against H, A & B.
Discovered in Bombay (Mumbai), India in the year 1952
Can donate blood to anybody with ABO grouping but can only receive blood from Bombay blood group people.
P, P1, Pk
P - signal transduction associate with cell adhesion
Pk - for B cell differentiation & precursor for P (rare individual not convert Pk to P)
On RBC and surface of urinary tract
Produced by a) gene B3GALNTI (at 22q13.2)
b) gene A4GALT (at 3q26.1)
Antibodies involved: IgM, IgG
80% P (P1), G (P1,P)
20% P (P2), G (P)
<1 % P (Pk1), G (P, Pk1)
P (Pk2), G (Pk
P (P) G (N/A)
Lewis blood group
Lewis antigens are secreted into the body fluids and absorbed onto the surface of erythrocytes.
Inherit Le gene = Lea
Two main types of Lewis antigen which are Lewis a (Lea) or Lewis b (Leb).
Three common phenotypes: Le(a+b-), Le(a-b+), and Le(a-b-).
Primary antibody is IgM
Prevalence : European : Antigen: (20% Lea), & 70% Leb on RBC
Discovered: Lea in 1946, Leb in 1948
Inherit both Le and Se gene = Leb
Kell Blood Group
3rd potent immunogenic antigen
Mrs. Kellacher (erythrocyte of her newborn infant-hemolytics reactions)
Cause hemolytic disease of fetus, HDFN & hemolytics transfusion reaction (HTR)
Discovered in 1946, inside the serum of Mrs. Kellacher
Antibody : IgG, predominant is IgG1
Lutheran Blood Group
A classification of blood based on the presence of Lutheran antigens.
It was first discovered in 1945.
The antigens arise from variations in gene called basal cell adhesion molecule (BCAM).
There are 19 known Lutheran antigens all together and 2 codominant alleles, Lua and Lub.
The most frequent phenotype is Lu(a-b+) while Lu(a-b-) is extremely uncommon
Antibody : Predominant IgM
Kidd Blood Group
The Kidd blood group was discovered in 1951.
Phenotypes: Jk(a+b-), Jk(a+b+), Jk(a-b+), Jk(a-b-)
Kidd antigens are expressed on a red cell transmembrane glycoprotein which transports urea across the red cells membrane
The two important antigens are: Jk a and Jk b
-other antigen: Jk3
Kidd antibodies are of IgG type that can activate complement (Anti-Jka, Anti-Jkb )
Stimulated by transfusion or pregnancy
Can cause Haemolytic Disease of the Newborn(HDNB)
They are also a very common cause of delayed Haemolytic Transfusion Reactions
Jk (a-b+)=22% &
Jk (a-b-)= exceedingly rare
MNSs Blood Group
Number of antigens:
42 including M, N, S, and s
Function of the molecules that carry the MNS antigens:
Glycophorins A and B may serve as receptors for cytokines, bacteria, and viruses and they bear the MNS antigens.
Anti-M : predominantly IgM and can be naturally occurring.
Can cause Hemolytic Disease of Newborn.
MNS: 2nd blood group that discovered in 1927, after immunizing rabbits with human RBCs.
Anti-N : very rare, similar reactivity as anti-M.
Most in kidney dialysis patient as cross-reacting antibody to formaldehyde.
Anti-S and Anti-s : form following red cell immunization due to transfusion and pregnancies. Usually IgG causing Hemolytic Transfusion Reactions (HTR) (delayed) and Hemolytic Disease of the Newborn (HDN)
FATIN NUR AZIRA BINTI AZHARI 1517302
NURUL AZAHANA BT MOHD NAYIAN 1515854
NOR ZUZIANA BINTI MD ZULKIFLI 1518504
NUR AMIRAH BINTE KAMARUZAMAN 1518886
NUR SURIANA BT MAH HASSAN 1514778
WAN ADILA FATINHAH BT WAN ZAINAL ABIDIN 1514670
SAMHANA BT SUHAILI 1517484
SITI SHAHIDAH BINTI SAYADI 1515100
NOR HIDAYAH BT EMI 1512684
P Blood Group