MAJOR BLOOD GROUPS

Lewis Blood Group

This blood group is not from RBCs but of the glycosphingolipids in the plasma that are passively adsorbed to the RBCs.

Le^a and Le^b

These antigens are thought to be antithetical, but they’re only a result of an interaction between 2 fucosyltransferases.

Le

This gene must be present for the precursor substance to be converted to Le^a.

Se

This gene must be present for the precursor substance to be converted to Le^b.

Le (a+)

These individuals are nonsecretors of ABH.

Le (b+)

These individuals are secretors of ABH.

Lea (a–b–)

This Lewis phenotype is more common in Africans.

Le (a+b+)

This Lewis phenotype is more common in Asians.

Anti-Lea

The most commonly encountered Lewis antibody.

80%

Le (a–b+)

What is the percentage of ABH secretors?

State the Lewis phenotype.

20%

Le (a+b-)

What is the percentage of ABH nonsecretors?

State the Lewis phenotype.

GI tract

This is thought to be the primary source of Lewis glycolipid in plasma.

10 days

Lewis antigens are not detectable in plasma until ___ after birth.

Birth: Le (a-b-)

After 10 days: Le (a+b-)

After 6 years: Le (a-b+)

State the transformation of Lewis phenotypes from birth to adulthood.

Le (a-b+)

What is the true Lewis phenotype?

lele genes

Individuals with this gene phenotype as Le (a-b-) from birth to the rest of their lives.

Le^a

This Lewis antigen is produced regardless of secretor status.

Lewis null

Formed due to a mutation; a non-functional or partially active Lewis phenotype.

• P

• P1

• Pk

• LKE

• PX2

• NOR

Traditional P Blood Group antigens, including the ones that were just added later on.

P1Pk: P1, Pk, NOR

Globoside: P and PX2

Currently, traditional P Blood Group antigens are assigned in which respective blood group?

• Anti-P1

• P1

• P2

• p

State the current terms used for each antigen and phenotype.

• Anti-P

• P(+) Phenotype

• P(-)

• P null

Pk

This antigen from P blood group is expressed in all RBCs except of the null phenotype.

P1 and P2

These phenotypes from P blood group is the two most common.

P, P1k, P2k

Three rare phenotypes from P Blood Group

Black

This ethnicity has a more common occurrence of P1.

• A4GALT

• B3GALNT1

Identify the genes:

• P1PK

• Globoside

• Binds at 4C

• Lyses at 37C

Anti-P in PCH

• ___ at 4C

• ___ at 37C

Luke (-)

Individuals with p and pk phenotype are what phenotype in LUKE.

PX2

It was added to the GLOB collection because it is a product of B3GALNT1.

The LKE antigen has a frequency of 98% and is found in all cord cells.

The LKE antigen has a frequency of ___ and is found in all ___ cells.

I Blood Group System

A cold agglutinin that was named by Wiener and coworkers.

• Not antithetical

• Reciprocal in terms of amount in age

Describe the relationship of I and i antigens.

I antigen is more abundant in adults, while i is in trace amounts.

i antigen is more abundant in infants.

How do I and i antigen show reciprocity?

• Incubation in cold

• Use of albumin

• Use of enzyme methods

How is anti-I reactivity enhanced?

Antigen i

This antigen is predominantly seen in fetal RBCs and decreases at 18 months of life.

GlcNAc and IGnT

The gene for I Blood Group System

• Leukocytes

• Platelets

• RBCs

• Plasma and Serum

• Human breast milk

• Saliva

• Amniotic fluid

I and i antigens are seen on the membrane(s) of?

Melanasians and Yanomami Indians

Benign Anti-I^T is seen in what population?

Glycophorin B

The major RBC sialic acid-rich glycoprotein.

M and N antigens

These antigens reside in Glycophorin A.

S and s antigens

These antigens reside in Glycophorin B.

M: serine at position 1, glycine at position 5

N: leucine at position 1, glutamic acid at position 5

How are M and N antigens differentiated based on the positions?

They are located at the outer end of GPA.

Why are M and N antigens easily destroyed by routine blood bank enzymes?

Neuraminidase

This enzyme cleaves sialic acid.

S: methionine at position 29

s: threonine at position 29

How are S and s antigens differentiated based on the positions?

They are located farther down the glycoprotein, where enzyme-sensitive sites are less accessible.

Why are S and s antigens less easily destroyed by routine blood bank enzymes?

Anti-M

These are IgM antibodies that do not bind complement.

• Children

• Patients with bacterial infections

Anti-M is more common in what population?

Anti-M

6.5 pH

This antibody is pH-dependent. State the pH level wherein it reacts best.

Anti-M

This antibody only react with RBCs exposed to glucose solutions.

U- phenotype

This phenotype is seen in individuals who lack GPB because of partial or complete deletion of GYPB. They type as S-s-U-.

U^var (U variant)

This phenotype have altered GPB that does not express S or s.

En(a-) Phenotype

This phenotype is seen in individuals with M-N- and reduced NeuNac gene.

Mk Phenotype

This phenotype is a rare, silent gene at Ss locus. They type as M-N-S-s-U-En(a-)Wr(a-b-).

Mk Phenotype

It is a single, near-complete deletion of both GYPA and GYPB.

M^kM^k

The null phenotype in MNS system.

Kell Blood Group

The first blood group system discovered after the introduction of antiglobulin testing.

• Kp^a

• Kp^b

• Js^a

• Js^b

• K₀

State the antigens seen in KELL.

KELL Blood Group

This blood group system is seen only in RBCs.

1. ABO

2. D

3. KELL

State the ranking of immunogenicity between antigens.

Glycine acid EDTA

This IgG removal agent destroys Kell antigens.

Low: Kp^a, Kp^c, Js^a

High: Kp^b, Js^b

In KELL Blood group, state the low prevalence and high prevalence antigens.

Antiglobulin testing

The most reliable detection method for Kell.

Kell

It is a member of the neprilysin family of zinc peptidases.

Xk gene

This gene encodes the Kx antigen and is independent of KEL. It is located at the short arm of the X chromosome.

Kx

This antigen is present on all RBCs except of those with McLeod phenotype.

Anti-Ku

The antibody made by K₀ phenotypes.

McLeod phenotype

This phenotype is sex-linked, wherein males are the only ones who are affected. Females are only carriers.

• Acanthocytic

• Possibility of Chronic Granulomatous Disease

• Chronic but well-compensated HA

  • reticulocytosis

  • splenomegaly

  • bilirubinemia

  • reduced serum haptoglobin

State the clinical manifestations of McLeod phenotype individuals.

McLeod Syndrome

Characterized by muscular dystrophy and cardiomegaly, along with neurological disorders such as areflexia and choreiform, resulting in increased CK-MM.

Duffy Blood Group System

Found in a multiply transfused hemophiliac.

Duffy glycoprotein

It is a member of the superfamily of chemokine receptors and is known as the atypical chemokine receptor 1.

Duffy gene

ACKR1 or DARC, Chromosome 1

The first human gene to be assigned to a chromosome.

State the specific gene and its associated chromosome.

Fy

The gene in Duffy null phenotype.

Anti-Fy^a

This antibody occurs 3x less than Anti-K.

Fyx

An inherited, weak form of Fyb.

Kidd Glycoprotein

This is the RBC Urea transporter, which maintains the osmotic stability and shape of RBCs. It is also expressed in the kidneys.

Anti-Jk^a

This Kidd antibody is more frequently encountered.

Kidd null

This phenotype lacks Jk^a, Jk^b, and the common antigen Jk3.

Kidd null

This phenotype was seen in Filipinos.

Anti-Lu^a

Seen in the serum of patient with lupus erythematosus.

Anti-Lu^a: IgM

Anti-Lu^b: IgG

The difference between Lutheran antibodies regarding immunoglobulin class.

BCAM; Chromosome 19

Lutheran gene. State its corresponding chromosome.

• Kidd

• Duffy

• Kell

Blood Groups whose autoantibodies have mimicking specificity.