OTHER BLOOD
GROUPS SYSTEM
DAYLE DANIEL SORVETO, RMT
PRINCESS ALEN AGUILAR, RMT
Lewis Antigens
Soluble antigens produced by tissues and found in body fluids (plasma)
Adsorbed on the RBC
Lewis substance adheres to RBC
becoming an antigen
RBC
Le substance in plasma
Le genes
Lewis inheritance
Lewis system depends on Hh, Se, and Le genes
le, h, and se do not produce products
If the Le gene is inherited, Lea substance is produced
Le, H, and Se genes must ALL be inherited to convert Lea to Leb. Examples:
Le se H Le(a+b-)
Le Se H Le(a-b+)
le H se Le(a-b-)
le hh se Le(a-b-)
Lewis Antibodies
Usually occur naturally in those who are Le(a-b-)
Other phenotypes RARELY produce the antibody
IgM (may fix complement, becoming hemolytic)
Enzymes enhance activity
May be detected soon after pregnancy because pregnant women may temporarily
become Le(a-b-)
No clinical significance…Why?
Le antibodies in a patient can be neutralized by the Lewis antigens in the donor’s plasma
(cancel each other out)
do not cause HDN because they do not cross placenta (antigens not developed well in cord
blood)
Le(a-b-)
MNS antigen
ISBT 002 –chromosome 4(q28-q31)
M,N antigens associated w/glycophorin A
Easily destroyed by enzymes
S,s and U antigens associated w/glycophorin B
Important markers in paternity testing
Found on red cells, not in body fluids and secretions
M,N,S,s not found on platelets , lymphocytes, monocytes and granulocytes.
GPA, M & N have been detected on renal capillary endothelium and epithelium
Frequency of MNSs antigens
Phenotypes Blacks (%) Whites (%)
M+ 74 78
N+ 75 72
S+ 30.5 55
s+ 94 89
U+ 99 99.9
Anti-M and N
Anti-M is a relatively common ‘naturally • seen in renal patients, who are dialyzed on
occurring’ antibody, saline agglutinins that equipment sterilized with formaldehyde.
react below 37⁰c. Can demonstrate dosage. called anti-Nf
mostly IgM; however, they frequently contain
an IgG component. • Though it is clinically insignificant, it has been
They do not bind complement & do not react associated with rejection of a chilled
with enzyme treated RBC’s. transplanted kidney.
It appears to be more common in children
and in patients with burns.
Anti-M is rarely clinically significant;
hemolytic anti-M is usually IgG and reactive
at 37ºc.
anti M are ph dependent, reacting best at ph
6.5.
anti S & anti s
Antibodies to S, s, and U usually occur after exposure to
allogeneic red cells. All are capable of causing HTRs and HDFN.
Anti-S and -s are generally IgG antibodies active at 37°C.
These antibodies may are may not react with enzyme treated
RBC’s depending on extent of treatment.
Kell System
Similar to the Rh system Kp antigens
2 major antigens (over 20 exist) • Kpa is a low frequency
K (Kell), <9% of population antigen (only 2%)
k (cellano), >90% of population • Kpb is a high frequency
The K and k genes are codominant alleles on chromosome 7 antigen (99.9%)
that code for the antigens Js antigens
Well developed at birth • Jsa (20% in Blacks, 0.1% in
The K antigen is very immunogenic (2nd to the D antigen) in Whites)
stimulating antibody production • Jsb is high frequency (80-
Other Kell antigens 100%)
Other sets of alleles also exist in the Kell system:
Analogous to the Rh system: C/c and E/e
Kell
Kx antigen
antigens
Not a part of the Kell system, but is related
Kx antigens are present in small amounts in individuals with normal Kell antigens
Kx antigens
Kell arehave
antigens increased in those whoregions
disulfide-bonded are K0 on the glycoproteins
McLeod Syndrome
This makes them sensitive to sulfhydryl reagents:
TheXK1
2-mercaptoethanol
gene (on the (2-ME)
X chromosome) codes for the Kx antigen
Dithiothreitol (DTT)
When the gene is not inherited, Kx is absent (almost exclusive in White males)
2-aminoethylisothiouronium bromide (AET)
Causes abnormal red cell morphologies and decreased red cell survival:
Kellnull
or K–0spur cells (defected cell membrane)
Acanthocytes
Reticulocytes
No expression– immature
of Kell antigens except a
red cells related antigen called Kx
As a result
Associated withof transfusion, K0 individuals can disease
chronic granulomatous develop anti-Ku (Ku is on RBCs that
have Kell antigens)
WBCs engulf microorganisms, but cannot kill (normal flora)
Rare Kell negative units should be given
Kell antibodies
IgG (react well at AHG)
Produced as a result of immune stimulation (transfusion, pregnancy)
Clinically significant
Anti-K is most common because the K antigen is extremely
immunogenic
k, Kpb, and Jsb antibodies are rare (many individuals have these
antigens and won’t develop an antibody)
The other antibodies are also rare since few donors have the antigen
Kidd Blood Group
2 antigens
Jka and Jkb (codominant alleles)
Show dosage
Genotype Phenotype Whites (%) Blacks (%)
JkaJka Jk(a+b-) 26.3 51.1
JkaJkb Jk(a+b+ 50.3 40.8
JkbJkb Jk(a-b+) 23.4 8.1
JkJk Jk(a-b-) rare rare
Kidd
Kidd antibodies
Antigens
• Anti-Jk a and Anti-Jkb
Well developed at birth
IgG by enzymes
–Enhanced
– Clinically significant
Not very acessible on the RBC membrane
– Implicated in HTR and HDN
– Common cause of delayed HTR
– Usually appears with other antibodies when detected
• Anti-Jk3
– Found in some individuals who are Jk(a-b-)
– Far East and Pacific Islanders (RARE)
Duffy Blood Group
Predominant genes (codominant alleles):
Fya and Fyb code for antigens that are well developed at birth
Antigens are destroyed by enzymes
Show dosage
Phenotypes Blacks Whites
Fy(a+b-) 9 17
Fy(a+b+) 1 49
Fy(a-b+) 22 34
Fy(a-b-) 68 RARE
Duffy antibodies
The Duffy and Malaria Connection
• Most
IgG
African-Americans are Fy(a-b-)
• Interestingly, certain malarial parasites (Plasmodium
Do not bind complement
knowlesi and
Clinically significantP. vivax) will not invade Fy a and Fyb
negative
Stimulated bycells
transfusion or pregnancy (but not a common cause
• It ofseems
HDN)
either Fya or Fyb are needed for the
Do not react with enzyme treated RBCs
merozoite to attach to the red cell
• The Fy(a-b-) phenotype is found frequently in West
and Central Africans, supporting the theory of
selective evolution
