IMMUNOHEMATOLOGY

BLOOD GROUPS
Prepared by : Mark Wilson G. Lozada, RMT

✓ Other Blood Groups

o No Dosage / not affected by enzymes
▪ Kell (006)
• History
o 1st blood group system after the introduction of the antiglobulin
testing
o Anti-K was identified in 1946 in the serum of Mrs. Kelleher
• Antigens
o Consists of 36 high prevalence and low prevalence antigens
o K or KEL 1 and k or KEL2 (antithetical antigen)
▪ K antigen can be detected on fetal RBCs as early as 10
weeks whereas k antigen has been detected at 7 weeks
▪ K antigens immunogenicity is next to D antigens
o KEL 3 : Kpa | Penny
o KEL 4 : Kpb | Rautenberg; higher frequency than KEL3 and KEL
21
o KEL 5 : Ku
o KEL 6 : Jsa | Sutter
o KEL 7 : Jsb | Matthews
o KEL 21 : Kpc | Antithetical to Kpa and Kpb ; rare
• Biochemistry
o Antigens are located on a glycoprotein integral to rbc membrane
o Kell glycoprotein covalently linked to Kx
o Destroyed by Sulfhydryl Reagents such as dithiotreitol (DTT), 2-
mercaptoethanol, and 2-aminoethylisothiouroniumbromide (AET)
o ZZAP (contains DTT and papain)
o Also destroyed via combination of trypsin and chymotrypsin
o Not destroyed by Papain or Ficin
• Antibodies
o IgG
o Anti-K | most commonly seen antibody in blood bank; next only
to ABO and Rh antibodies ; detected through IAT; PEG can
increase reactivity
o Associated with HTR and HDFN
o Not affected by enzymes
▪ Kx (019)
• Absence of Kx antigen results in reduced expression of Kell antigens
o McLeod Phenotype
▪ Exclusive in males
▪ Produce anti-KL (antiKx and anti-Km)
▪ Acanthocytosis
▪ Well compensated hemolytic anemia
o McLeod Syndrome
▪ Elevated CK
▪ X-linked Chronic Granulomatous Diseases
• Increased expression in K0
• Not affected by Enzymes
▪ Lutheran
IMMUNOHEMATOLOGY
BLOOD GROUPS
Prepared by : Mark Wilson G. Lozada, RMT

• Linked to adhesion properties and intracellular signaling

• Primary antigens : Lua and Lub
o 20 antigens (other examples include the Aurberger antigens Aia
and Aub)
• Antibodies
o Anti-Lua may be naturally occurring; IgM/IgG class
▪ Rarely significant in transfusion
o Anti-Lub : IgG
o Exhibits Dosage / Affected by Enzymes
▪ Duffy Blood Group
• receptor for inflammatory chemokines
• Antigens
o Fya and Fyb
▪ Absence = resistance to P. vivax or P. knowlesii
o Fy3 : on cord cells; expressed only if Fya and Fyb are present
o Fy5 : similar to Fy3 except its association with Rh
o Fy6 : similar to Fy3 but destroyed by enzymes
• Antibodies are IgG
• Destoyed by Enzymes except Fy3 and Fy5
• Exhibits Dosage
▪ Kidd Blood Group
• Jka Jkb and Jk3
o Absence of Jka and Jkb = more resistant to lysis of 2M urea
▪ Typical to Polynesians Filipinos and Chinese
• Some antibodies may bind complements
• Antibody detection aided with enzyme reagents
• Exhibits dosage
▪ S,s,U
• GPYB gene
• Glycophorin B
o 72 aa with 43 outside cell membrane
o S and s differ at aa29
▪ S : methionine
▪ s : threonine
o U antigen is located near membrane; always present when S or
s is inherited
• IgG antibodies
o Affected by Enzyme / No Dosage
▪ GLOBOSIDE : P, PX2 (028) | LKE (209)
• P, LKE, PX2 antigens
• High frequency antigen
• P negative individuals may become sensitized upon contact with certain
parasites (eg. Tapeworms causing hydatid disease – Echinococcus
granulosus)
• Tilia leaf and flower of these plants contain P-like substance that can be
used as immunogen in the production of anti-P
• PX2 strongly expressed on p phenotype
o Anti-PX2 – naturally occurring
IMMUNOHEMATOLOGY
BLOOD GROUPS
Prepared by : Mark Wilson G. Lozada, RMT

• Reactivity of antibodies enhanced by enzyme treatment

• Autoanti-P
o Paroxysmal cold hemoglobinuria
o Biphasic hemolysin
o Donath-landsteiner anibody
o Not Significant
▪ M and N
• Not affected by enzymes; exhibits dosage
• GYPA gene
• Glycophorin A (GPA) – sialoglycoprotein
o 131 aa with 72 outside cell membrane
o M and N differ in aa position 1 and 5
o M : serine and glycine
o N : leucine and glumatic acid
• Anti-M IgM/IgG
• Anti-N : IgM
o Anti-N like activities – px exposed to formaldehyde-sterilized
dialyzer membranes
▪ I
• Enhanced by enzymes
• I gene : N-acetylglucosaminyltransferase
• I and i are not antithethical
• I and i exist on the precursor of A B H
o I : branched
o i : linear
o may be found on human milk and amniotic fluid
• Anti-I is IgM
• Autoanti-I : cold agglutinin / M. pneumoniae
• Anti-i : EBV-IM
▪ P1PK
• Enhanced by enzymes/ var dosage
• Pk precursor of P
o Addition of galactose to lactosylceramide
o Precursor of P
▪ P : N-acetylgalactosamine + Pk (different blood group)
• P1 antigen : D-galactose + type 2 precursor
o Found on hydatid cyst fluid
• P1 PHENOTYPE : expres P, P1, PK
o No antibodies
o Most common
o P1 ag not well developed at birth
• P2 PHENOTYPE : lacks P1
o Anti-P1 : IgM not clin sig
• anti Tja / anti PP1PK
▪ IgG
▪ Sig; assoc with spontaneous abortion
o anti Tja / anti PP1PK
▪ Lewis Blood Group
IMMUNOHEMATOLOGY
BLOOD GROUPS
Prepared by : Mark Wilson G. Lozada, RMT

• Enhanced by enzymes; No dosage

• Not synthesized by the RBCs
• Manufactured by tissue cells and secreted into body fluids
• Inheritance of Lewis antigen is dependent on the inheritance of lewis
genes as well as secretor gene
• Lewis antigens produced in saliva and other secretions are glycoproteins;
Lewis cell-bound antigens absorbed from plasma onto the RBC
membranes are glycolipids
• Nonsecretors – Le(a+b-) / (Le(a-b-) ; secretors (a-b+)
• Gene Product :
o Le, FUT3
▪ L-fucose to carbon 4 of NAG of type 1 precursor chains
or H chains in secretions
▪ Note : To mark the difference from FUT1, FUT1 of H
blood group adds L-Fucose on Galactose
o Se FUT2
• Lea antigen
o FUT3 adds Fucose on type 1 precursors and this lewis antigen is
adsorbed in RBC membrance creating this phenotype
o Structure : Type 1 Precursor + Fucose on NAG
o Cannot be converted to Leb
• Leb antigen
o FUT3 adds Fucose to type 1 H-structures in secretions (made
possible by Se gene which allows secretion of H antigens) aside
from type 1 precursor chains; however those H structures added
with fucose are adsorbed more preferentially on rbc
membrances
o Structure : H structure + Fucose on NAG
o Receptor of H. pylori and Norwalk virus
• Le and Leb are not alleles, rather, they result from the interaction of
a

two fucosyltransferases encoded by independent genes, Le and Se

Gene Antigens in Secretions Red Cell Phenotype
Le sese H Lea Le(a+b-)
Le Se H Lea Leb H Le(a-b+)
lele sese H None Le(a-b-)
lele Se H H Le(a-b-)
Le sese hh Lea Le(a+b-)
Le Se hh Lea Le(a+b-)
lele sese hh None Le(a-b-)
lele Se hh None Le(a-b-)