MIDTERM LECTURE L1: THE MNS SYSTEM Flashcards

1
Q

MNS system ISBT

A

002

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2
Q

Landsteiner and Levine found new antigen specificities by immunizing rabbits with

A

human RBCs

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3
Q

Anti-M and anti-N were discovered from the rabbit sera in what year

A

1927

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4
Q

T/F: M and N are antithetical antigens

A

T

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5
Q

Who discovered S antigen

A

Walsh and Montgomery

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6
Q

In what year was S antigen discovered

A

1947

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7
Q

Antithetical partner of S antigen

A

s antigen

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8
Q

s antigen was discovered in what year

A

1951

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9
Q

There is equilibrium/disequilibrium(?) in the expression of S and s with M and N.

A

disequilibrium

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10
Q

In white populations, what is the order of relative frequency for common MNS blood group system haplotypes? (MOST- LEAST frequent)

A

Ns > Ms > MS > NS

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11
Q

In 1953, which scientist named an antibody to the high-prevalence antigen U?

A

Wiener

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12
Q

U stands for

A

for almost UNIVERSAL distribution

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13
Q

The inclusion of U into
the MNS system was due to the observations of which scientist

A

Greenwalt and colleagues

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14
Q

What did Greenwalt and his colleagues observed?

A

All U– RBCs were also S–s–

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15
Q

How many antigens have been included in the MNS system?

A

46 antigens

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16
Q

MNS is almost equal in antigen size and complexity to what blood group system

A

Rh

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17
Q

The genes encoding the MNS antigens are located on what chromosome?

A

chromosome 4

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18
Q

The M and N antigens are found on a well-characterized
glycoprotein called

A

Glycophorin A (GPA)

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19
Q

Major RBC sialic acid–rich glycoprotein (sialoglycoprotein, SGP)

A

Glycophorin A (GPA)

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20
Q

The M and N antigens are antithetical and differ in their amino
acid residues at positions

A

1 and 5

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21
Q

M amino acid at position 1

A

serine

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22
Q

M amino acid at position 5

A

glycine

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23
Q

N amino acid at position 1

A

leucine

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24
Q

N amino acid at position 5

A

glutamic acid

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25
Q

There are about how many copies of GPA per RBC

A

about 10^6 copies

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26
Q

T/F: MNS are not well developed at birth

A

F (they’re well developed at birth)

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27
Q

T/F: M and N are located at the outer end of GPA

A

T

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28
Q

M and N are easily destroyed by what routine blood bank enzymes and less common enzymes?

A

routine blood bank enzymes
- ficin
- papain
- bromelin

less common enzymes
- trypsin
- pronase

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29
Q

Can MNS antigens be destroyed by DTT alone?

A

NO (needs ficin and papain)

DTT + f + p = ZZAP

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30
Q

Cleaves sialic acid

A

neuraminidase

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31
Q

neuraminidase is also known as

A

neuraminic acid or NeuNAc

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32
Q

M and N antibodies are homogenous/heterogeneous(?)

A

heterogenous

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33
Q

M and N antigens are detected on what tissues

A

renal endothelium, and epithelium

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34
Q

S and s antigens are located on a smaller glycoprotein called

A

glycophorin B (GPB)

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35
Q

S and s are differentiated by the amino acid at what position on GPB?

A

position 29

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36
Q

Amino acid that defines S

A

methionine

37
Q

Amino acid that defines s

38
Q

How many copies of GPB per RBC

A

about 200,000

39
Q

There are about how many times more copies of GPB on S+s– RBCs than on S–s+ RBCs?

A

1.5 times more copies

40
Q

Are S and s well developed at birth?

41
Q

T/F: S and s antigens are less easily degraded by enzymes
because the antigens are located farther down the glycoprotein

42
Q

S and s antigens have enzyme-sensitive sites that are less/more(?) accessible.

43
Q

Enzymes that destroy S and s acitivity

A
  • Ficin
  • papain
  • bromelin
  • pronase
  • chymotrypsin
44
Q

T/F: Trypsin does not destroy the S and
s antigens, and neither does DTT, AET, chloroquine, or
glycine-acid EDTA treatment.

45
Q

Is Anti-M naturally occurring?

46
Q

Anti-M is mostly what class of immunoglobulin?

47
Q

Anti-M is how many percent of IgG

48
Q

Does Anti-M bind complement?

A

No, regardless of their immunoglobulin class

49
Q

Does anti-M react with enzyme-treated RBCs?

50
Q

Anti-M is more common in children/adult(?)

51
Q

Anti-M is more common in patients with

A

bacterial infection and burns

52
Q

Anti-M is pH dependent. What pH?

53
Q

Anti-M lectin

A

Iberis amara

54
Q

T/F: As long as anti-M reacts at 37°C, it is clinically
significant for transfusion.

A

F (As long as anti-M doesn’t react at 37°C, it is not clinically
significant for transfusion and can be ignored)

55
Q

Does anti-M often cause HTRs, decreased cell survival, and HDFN?

A

no (it RARELY)

56
Q

Anti-N is cold/hot(?) reactive

57
Q

Anti-N immunoglobulin class

A

IgM and IgM

58
Q

Is anti-N clinically significant?

A

No, not clinically significant

59
Q

Does Anti-N bind complement?

A

No, it doesn’t

60
Q

Anti-N is seen in which patients

A

renal patients

61
Q

What substance may alter the M and N antigens?

A

formaldehyde

62
Q

Anti-N lectin

A

▪ Vicia graminea,
▪ Bauhinia variegate
▪ Bauhinia purpura

63
Q

Anti-S and anti-s are mostly what immunoglobulin class?

A

Mostly IgG

64
Q

Anti-S and anti-s are reactive at what temperature

65
Q

Can anti-S and anti-s bind to complement?

66
Q

A few of anti-S and anti-s express optimal reactivity between 10°C and 22°C by what test

A

saline indirect antiglobulin test

67
Q

If anti-S or anti-s specificity is suspected but the pattern of reactivity is not clear, what can you do that can help in identification?

A

incubating tests at RT and immediately performing the antiglobulin test (without incubating at 37°C)

68
Q

T/F: Dosage effect can be exhibited by many examples of anti-S and anti-s, but not as dramatic as seen with anti-M and anti-N

69
Q

Only how many percent of whites are s–?

A

11% of whites

70
Q

Only how many percent of blacks are s–?

A

3% of blacks

71
Q

S– units/s- units(?) are much easier to find

72
Q

How many percent of whites are S–?

A

45% of whites

73
Q

How many percent of blacks are S–?

A

69% of blacks

74
Q

phenotype with partial/complete deletion of GPB

A

U-phenotype (Universal)

75
Q

U-phenotype (Universal) immunoglobulin class

76
Q

Can U-phenotype (Universal) cause severe HTR and NDN?

77
Q

RBCs of individuals with U-phenotype type?

78
Q

phenotype with gene deletion of GPA

A

En (a-) phenotype (envelope)

79
Q

rare and silent phenotype

A

Mk phenotype (null)

80
Q

Mk phenotype was named by

A

Metaxas and Metaxas-Buhler

81
Q

In what year did Metaxas and Metaxas-Buhler find an allele that does not produce M or N

82
Q

RBCs of individuals with Mk phenotype type?

A

M–N–S–s–U–En(a–)Wr(a–b–)

83
Q

MNS phenotype common in blacks

A

U-phenotype

84
Q

En (a-) phenotype is resistant to what infection

A

Pasmodium vivax

85
Q

Who discovered En phenotype

A

Darnborough and cowrkers

and

Furuhjelm and colleagues

86
Q

En(a-) phenotype was discovered in what year

87
Q

En(a–) individuals appeared to have RBCs typed as?

A

M–N– with reduced NeuNAc

88
Q

Most En(a–) individuals produce what antibody

89
Q

What parasite appears to use alternative receptors, including GPA and GPB for cell invasion?

A

Plasmodium falciparum