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:
 TheXK1
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