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[Immunohematology] Lec > OTHER BLOOD GROUP SYSTEMS PART 1 (LEWIS, P, LUKE) > Flashcards

OTHER BLOOD GROUP SYSTEMS PART 1 (LEWIS, P, LUKE) Flashcards

1
Q

Antigens in the Lewis blood group system do not develop as integral parts of the red blood cell (RBC) membrane. Instead, they are adsorbed by the [?].

A

RBCs from the surrounding plasma

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2
Q

• The amount of Lewis antigen varies and depends on:

• Individual’s (?).
• Gradual development of (?).
• Influence of (?) genes.

A

ABO phenotype and age
Lewis Ag
H, Se, and Le

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3
Q

• Lewis antigen expression may decrease dramatically during.

A

pregnancy

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4
Q

Lewis

The most common phenotypes include:

A

• Le(a+b−)
• Le(a−b+)
• Le(a+b+)
• Le(a−b−)

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5
Q

• Most neonates typically type as [?] regardless of inherited Lewis genes.

A

Le(a−b−)

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6
Q

• Usually IgM but may contain IgG components.

A

Anti-Lea antibodies

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7
Q

• React best at room temperature but may also react at 37°C.

A

Anti-Lea antibodies

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8
Q

• Can bind complement and trigger in vitro hemolysis, potentially causing hemolytic transfusion reactions (HTR).

A

Anti-Lea antibodies

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9
Q

• Anti-Lea or Anti-Leb

is enhanced by enzyme treatment.

A

Anti-Lea or Anti-Leb

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10
Q

• Usually IgM and react best at room temperature.

A

Anti-Leb antibodies

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11
Q

• Bind complement poorly.

A

Anti-Leb antibodies

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12
Q

• Activity is enhanced by enzyme treatment.

A

Anti-Leb antibodies

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13
Q

• Lewis antibodies may transiently appear during pregnancy in [?] women but disappear after delivery.

A

Le(a−b−)

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14
Q

• Both [?] react with most cells on routine RBC panels.

A

anti-Lea and anti-Leb antibodies

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15
Q

• Lewis substance can neutralize these antibodies, allowing the detection of other antibodies present.

A

anti-Lea and anti-Leb antibodies

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16
Q

• Poorly developed at birth: Lewis antigens are not fully developed in.

A

newborns

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17
Q

• Reversibly adsorbed onto red cells from plasma: can attach to the surface of red blood cells from the plasma and can be removed under certain conditions.

A

Lewis antigens

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18
Q

• Not found on cord blood or newborn red cells (Le(a-b-)): Cord blood and newborn red cells typically lack the antigens initially.

A

Lewis

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19
Q

• Lewis glycolipids detectable in plasma after approximately [?]: It takes around 10 days after birth for Lewis glycolipids tobecome detectable in the plasma.

A

10 days of life

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20
Q

• Transformation of Lewis phenotype after [?]: Individuals may undergo changes in their Lewis phenotype after birth, transitioning from Le(a-b-) to the true phenotype, which is Le(a-b-).

A

birth

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21
Q

• Decrease in expression during [?]: Expression of Lewis antigens on red blood cells can decrease in pregnant women, leading to a Le(a-b-) phenotype during pregnancy.

A

pregnancy

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22
Q

Do not exhibit dosage effects in serologic reactions. This means that the presence of one or two copies of the gene does not affect the strength of the antigen reaction in serological testing.

A

Lewis antigens

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23
Q

• Naturally occurring: are typically present in the serum without prior sensitization to foreign antigens.

A

Lewis antibodies

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24
Q

• Predominantly IgM: These antibodies are primarily of the IgM class, which means they are relatively large and can agglutinate red blood cells efficiently.

A

Lewis

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25
Q

• May cause in vivo hemolysis

A

Lewis antibodies

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26
Q

•Synthesis and Structure: Lewis blood group antigens are produced by tissue cells and secreted into body fluids.Those in secretions are [?], while those absorbed onto red blood cell membranes are [?].

A

glycoproteins

glycolipids

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27
Q

•Genetic Basis: The Le gene codes for [?], necessary for Lea expression, while Le and Se genes are needed for Leb expression.

A

L-fucosyltransferase

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28
Q

•Antigen Formation: Lea antigen is formed by adding [?] to a specific carbon of [?], while Leb antigen requires a second addition of L-fucose to a specific carbon of N-acetylglucosamine.

A

L-fucose

N-acetylglucosamine

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29
Q

•Phenotypes andSecretor Status: Le(a-b-) individuals are [?] and have only [?], while Le(a-b+) individuals are [?] and have both [?].

A

ABH nonsecretors; Lea substance

ABH secretors; Lea and Leb substances

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30
Q

The most common phenotype in both white and black populations is [?], with the [?] being more common among blacks.

A

Le(a-b-)

lele genotype

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31
Q

are poorly expressed at birth and do not exhibit dosage effects in serologic reactions.

A

Lewis antigens

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32
Q

•Antibodies: Lewis antibodies, typically [?] and [?], can bind [?] and are enhanced by [?].

A

IgM; naturally occurring

complement; enzymes

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33
Q

Lewis substance in [?] can neutralize these antibodies. They are frequently encountered in [?] but are not considered significant in [?].

A

secretions

pregnant women

transfusion medicine

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34
Q

• Traditionally, the P blood group included [?].

A

P, P1, Pk antigens, and later, Luke (LKE)

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35
Q

• In the [?] nomenclature:

A

International Society of Blood Transfusion (ISBT)

36
Q

are assigned to the P1Pk blood group system

A

• P1 and Pk antigens

37
Q

is assigned to the globoside blood group system

A

• P antigen

38
Q

(003, P1PK).

A

• P1 and Pk antigens

39
Q

(028, symbol GLOB).

A

• P antigen

40
Q

are assigned to the Globoside Collection

A

• LKE and PX2

41
Q

(029, GLOB)

A

• LKE and PX2

42
Q

• The P1PK gene is located at chromosome

A

22q11.2.

43
Q

• The Pgene is located at chromosome

A

3q26.1.

44
Q

• Biosynthetic Pathways: There are two distinct pathways for synthesizing P blood group antigens.

A

• Pathway on the left results in paragloboside and P1 antigens

• Pathway on the right leads to the production of the globoside series: Pk, P, and LKE antigens.

45
Q

• Common precursor:

A

Lactosylceramide (or Gb2, also known as ceramide dihexose or CDH).

46
Q

is also a precursor for the ABH antigens.

A

Paragloboside

47
Q

• Pathway on the right leads to the production of the globoside series:

A

Pk, P, and LKE antigens.

48
Q

: Common phenotype (about 75% of the population) with both P and P1 antigens.

is well developed at birth

is poorly developed at birth.

A

1.P1 Phenotype

P antigen

P1 antigen

49
Q

: Common phenotype, individuals have only P antigen.

A

2.P2 Phenotype

50
Q

: Very rare, individuals have both P1 and Pk antigens.

A

3.Pk1 Phenotype

51
Q

: Very rare, individuals have both P2 and Pk antigens.

A

4.Pk2 Phenotype

52
Q

: Extremely rare, RBCs are negative for P, P1, and Pk antigens.

A
  1. p Phenotype
53
Q

: Naturally occurring, cold-reacting, IgM antibodies often found in individuals with P2 phenotype.

A

1.Anti-P1 Antibodies

54
Q

Rarely react at temperatures higher than room temperature, but they can bind complement.

A

1.Anti-P1 Antibodies

55
Q

Not associated with hemolytic disease of the newborn (HDN) and rarely cause hemolytic transfusion reactions (HTR).

A

1.Anti-P1 Antibodies

56
Q

Produced by individuals with Pk1 or Pk2 phenotypes, can cause severe HTR.

A
  1. Anti-P Antibodies
57
Q

[?], also known as the Donath-Landsteiner antibody

A

Autoanti-P

58
Q

is a cold-reacting antibody associated with paroxysmal cold hemoglobinuria (PCH).

A

Autoanti-P

59
Q

3.Other Antibodies: occur only rarely.

A

Anti-PP, anti-Pk, and anti-p antibodies

60
Q

Discovered in 1965 by Tippett et al. in a patient with Hodgkin’s lymphoma.

A

Luke (LKE) Antigen and Antibody

61
Q

Luke (LKE) Antigen and Antibody Divides the population into three phenotypes:

A

Luke+, Luke(w), and Luke-.

62
Q

Approximately [?] of individuals are Luke+, [?] are weakly positive (Luke(w)), and [?] are Luke-.

A

84%

14%

2%

63
Q

Although it segregates independently of the P blood group, it is phenotypically related because the antibody reacts with most RBCs except those with rare P1, P2, p, and Pk phenotypes.

A

LKE

64
Q

Individuals with the [?] are always Luke- (or–LKE-).

A

p and Pk phenotypes

65
Q

LKE+ individuals can be either

A

P1 or P2.

66
Q

The Pk antigen is more strongly expressed on [?] than on LKE- RBCs.

A

LKE+ RBCs

67
Q

Only five examples of human [?] are known.

A

alloanti-LKE

68
Q

The original antibody was a saline agglutinin reacting best at– 4°C.

A

Luke (LKE) Antibody

69
Q

It became a potent hemolysin with enzyme methods and additional complement.

A

Luke (LKE) Antibody

70
Q

Other examples of [?] are much weaker and clinically insignificant.

A

alloanti-LKE

71
Q

have been associated with parasitic infections.

A

Anti-P1 antibodies

72
Q

• Antibodies such as [?] have been linked toearly abortions.

A

anti-PP1Pk or anti-P

73
Q

are implicated in causing PCH

A

• Autoanti-P antibodies

74
Q

a condition characterized by the sudden destruction of red blood cells in response to cold temperatures.

A

Paroxysmal Cold Hemoglobinuria (PCH)

75
Q

• Certain strains of Escherichia coli associated with urinary tract infections adhere to [?] on uroepithelial cells. This adherence facilitates their ascent in a ladderlike fashion through the urinary tract.

A

P1 and/or Pk glycolipids

76
Q

• Streptococcus suis, a bacterium that can cause meningitis and septicemia in humans, binds exclusively to

A

Pk antigen.

77
Q

• Toxins secreted by pathogens such as Shigella dysenteriae, Vibrio cholerae, Vibrio parahaemolyticus, and some pathogenic strains of E. coli have binding specificity for the [?].

A

Gal(α1-4)Gal(β1-4) moiety found in P1 and Pk antigens

78
Q

• Human parvovirus B19 uses [?] as a receptor for infection.

A

globoside

79
Q

•The P blood group comprises the antigens [?], which are biochemically related.

A

P, P1, Pk, andLKE

80
Q

•There’s a biochemical relationship between

A

the P blood group antigens and the ABH and I antigens.

81
Q

•Produced by all p individuals early in life without RBC sensitization.

A

Anti-PP1PkAntibody

82
Q

•Reacts with all RBCs except those of other p individuals.

A

Anti-PP1PkAntibody

83
Q

•Antibodies may be a mixture of IgM and IgG, efficiently bind complement, and may demonstrate in-vitro hemolysis.

A

Anti-PP1PkAntibody

84
Q

• Found as a naturally occurring alloantibody in the sera of all p

A

Anti-P Antibody

85
Q

• Usually caused by autoantibodies demonstrating anti-P specificity.

A

Paroxysmal Cold Hemoglobinuria (PCH)

86
Q

PCH autoantibodies are (?) hemolysins typically detectable only by the Donath-Landsteiner test.

A

IgG biphasic

[Immunohematology] Lec (35 decks)

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