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UNCOMMON Flashcards

1
Q

are missing on PNH III RBCs, which are devoid of all glycophosphoinositol (linked glycoproteins)

A

• Yt antigens are missing on PNH III RBCs, which are devoid of all glycophosphoinositol (linked glycoproteins)

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2
Q

-a high incidence antigen expressed by 99.8% of Caucasian donors

A

Yta

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3
Q

are expressed on RBCs, neural synapses, neuromuscular junctions

A

Cartwright antigens

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4
Q
  • Clinically benign
  • not associated with HDFN
  • arised from immune stimulation
  • shortened cell survival and delayed HTR
    -usually detected in iat
A

Anti-yta and anti-ytb

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5
Q
A
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6
Q
A
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7
Q

More likely to cause a monocytolayer asay with decreased cell survival

A

Anti-yta

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8
Q

Is a critical enzyme required for the rapid degradation of acetylcholine on postsynaptic membrenes of nerves and muscles

A

AChE(acetylcholinestorase)

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9
Q

Specific for RBC and Erythropoietic Tissues

A

Scianna

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10
Q

• the antigens are relatively resistant to enzymes but can be weakened with DTT and AET

A

Scianna blod group system

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11
Q

associated with warm autoimmune hemolytic anemia

A

Autoantibodies against Scl and Sc3 antigens

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12
Q

Is sciana associated with htr and hdfn?

A

No only hdfn

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13
Q

Which antibody of ISBT 013 is associated with HDFN

A

Anti-Sc4 and anti-Sc2
- have been associated with HDFN

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14
Q

• its structure suggests that it may play a role in RBC adhesion and signaling

A

ERMAP

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15
Q

• the Igy domain possesses a Clq recognition sequence that may mediate adhesion between marrow macrophages and erythroblasts in erythroid islands

A

ERMAP

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16
Q

could be involved in immune recognition and autoimmune anemia

A

ERMAP

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17
Q

Which part of ermap mediates adhesion between marrow macrophages and erythroblasts in erythroid islands

A

the Igy domain possesses a Clq recognition sequence

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18
Q
  • poor immunogens
  • mRNA has benn identified In: RBC, fetal liver and spleen
A

Dombrock

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19
Q

• high incidence antigens found on virtually all donors

A

Gya, Hy, Joa,DOYA, and DOMR

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20
Q

commonly found in mixturos of alloantibodies and can be difficult to identily

A

Dombrock

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21
Q

Isbt 014 whose antibody reactivity can be enhanced by the use of papain or ficin treated RBCS

A

Dombrock

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22
Q

antibody reactivity is reduced or abolished by the treatment of red cells with sulthydryl reducing ogents (DTT, AET), trypsin, chymotrypsin, pronase

A

Dombrock

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23
Q

• IgG, Immune Stimulation
• Clinically significant. many are benign
• capable of causing shortened RBC survival and acute and delayed hemolytic transfusion reactions

A

Dombrock

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24
Q

Can isbt 014 cause htr and hdfn

A

• capablo of causing shortened RBC survival and acute and delayed hemolytic transfusion reactions

Anti Dombrock is not associated with HDFN

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25
Q

can be observed in paroxysmal nocturnal hemoglobinuria type
III (PNH III)

A

Acquired Do null phenotype

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26
Q

characterized by chronic hemolysis due to an absence of all
GPI linked glycoproteins, including Cromer, Dombrock and
Cartwright antigens

A

paroxysmal nocturnal hemoglobinuria type
III (PNH III)

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27
Q

may play a role in clearing circulating NAD+ and/of posttranslational modification of proteins

A

Dombrock

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28
Q

may also contribute to integrin-mediated cell adhesion

A

Dombrock

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29
Q

What are the antigens of the colton blood group system

A

4 antigens: Coa, Cob, Co3, COA
• Coa high incidence Ag (937% donor)
* Cob 11% of donors; only 0.3% are Co (a b+) phenotype
* Co (a-b-) nuil Very rare
• Antibody against Co a

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30
Q

Located in the RBCS, PCT, descending LOH, renal vasa recta, endothellum, choroid plexus, ciliary body, microvessels, gall bladder, placenta & some epithelial calls

A

Colton blood group system

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31
Q

clinically significant antibodies associated with shortened red cell survival, HT& and HDFN

A

Colton

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32
Q

• immune antibodies
• can sometimes bind Complement

A

Colton

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33
Q

ISBT 015 is enhanced by

A

AHG, protease treatment

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34
Q

Expression of this antigen is dependent on RhD protein expression
Originated from the discovery of the D antigen

A

LW

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35
Q

Plasma origin,absorbed on rbc and is of high incidence

A

LW blood group

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36
Q

Lw

A

Expression of LW antigen is dependent on RhD protein expression
Originated from the discovery of the D antigen

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37
Q

Does lw cause htr and hdfn

A

• clinically benign antibodies, IgG, rarely cause HDFN and HTR

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38
Q

• agglutinates all cells except Rh null Cells

A

anti LW

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39
Q

•
• a potential counterreceptor for the b2 integrin protein Mac1(CD11b/CD18), LFA 1 (CDIla/CD18), and platelet GPIlb /IIIa

A

LW glycoprotein

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40
Q

may participate in adhesive interactions during early erythroid development

may also be involved in red cell senescence by binding to
CD11/CD18 integrin on splenic macrophages

A

LW glycoprotein

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41
Q

is elevated in sickle cell patients and may be involved in microvascular occlusion

A

LW

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42
Q

Does gerbich cause htr and hdfn

A

No

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43
Q

• of plasma origin and are passively adsorbed onto RBC membranes
• weakly expressed on cord RBCs and some GYPA deficient RBCs

44
Q

Rare reports of anaphylaxis plasma and platelet transfusion

45
Q

antibody reactivity can be enhanced by incubating ABCs in a low lonic sucrose solution

46
Q

antibody reactivity can be inhibited by plasma or by treatment of RBCS with proteases

47
Q

• NEUTRALIZATION: serum (contains complement)

49
Q

Its Glycoproteins are on: RBCs, Platelets, Kidneys, fetal Liver

50
Q

017

52
Q

• Decrease antigens in patients with horeditary elliptocytosis due to protein 41 deficienty

53
Q

Does gerbich cause htr and hdfn

A

cause delayed HTR and severe HDN

54
Q

causes low RBC viability

55
Q

resistant to enzymes (chymotrypsin), sensitive to protease (trypsin, pronase)

56
Q

• Autoantibodios associated with severe autoimmune hemolylic anomia

57
Q

deficiency Is associated with autoimmune disorders and susceptibility to bacterial meningitis

58
Q

specific allotypes have been linked to several autoimmune disorders, including rheumatoid arthritis and Graves’ disease

59
Q

similar to Diego/Band 3, help anchor the membrane to the underlying cytoskeleton

A

GYPC and GYPD

60
Q

in patients with protein 4.1 deficiency and hereditary elliptocytosis, it is decreased (75% normal)

A

GYPC and GYPD

61
Q

rich in sialic acid can bind influenza virus

A

GYPC and GYPD

62
Q

associated with marked elliptocytosis due to reduced membrane stability and deformability

A

Ge null (Leach) phenotype

63
Q

associated with decreased RBC survival and hemolytic transfusion reactions

64
Q

DELETE

A

associated with decreased RBC survival and hemolytic transfusion reactions

65
Q

Antigen of ISBT 021 associated with htr

A

anti Tc and anti Cr° have been implicated in HTR

66
Q

in several cases, a transient loss of_________ was noted in the second and third trimesters with reappearance of the antibody following delivery

A

anti Cromer antibodies

67
Q

can be inhibited by plasma, urine, and platelet concentrates

68
Q

• antibody reactivity is highly sensitive to pretreatment of RBCs with chymotrypsin and pronase, but not with other proteases

69
Q

protects cells from complement by promoting the decay of two
C3 convertases: C4b2a and СЗЬВЬ

70
Q

also a receptor for:

• uropathogenic and intestinal E. coli strains bearing Afa /Dr and X adhesins
• echovirus
• coxsackie B virus

71
Q

Null phenotype of ISBT 022

A

Helgeson Phenotype (Null Phenotype)

72
Q

are resistant to proteases but are weakened by sulfhydryl reducing agents (AET, DTT)

A

• Knops antigens

73
Q

ANTIBODIES
• IgG, immune stimulation
• Clinically insignificant
• Reactive in DAT

74
Q

complement regulatory protein
can bind C3b/Cab immune complexes, promoting their degradation by factor 1
also enhances

75
Q

could play a role in Leishmania, Legionella, and Mycobacterium infections

76
Q

• also binds P. (alciparum with rosette formation a clinical finding associated with severe malaria

78
Q

show reduced P. falciparum binding and rosetting

A

SI (a-) RBCs

79
Q

high frequency allele (99% white peoplo)

80
Q

with the exception of AnW], In Ag are destroyed by proteases and
AET

81
Q

• can be clinically significant, with shortened RBC survival and transfusion reactions

82
Q

are also inhibited by plasma, w/c contains soluble CD44

A

• Anti Indian

83
Q

Resistant to Enzymes, sialidases, sulfhydryl reducing agents

84
Q

ANTIBODIES
• IgG
• reactive in DAT
• does not cause HDFN
• decreased RBC survival

85
Q

Q on WBCs, is a leukocyte activation associated protein may participate in cell adhesion, tumorigenesis, and wound healing via stimulation of enzymes required for remodeling of the extracellular matrix

86
Q

may also play a role in the trafficking of red cells out of the spleen

87
Q

• Red cell aging is accompanied by progressive loss of CO|47, suggesting a possible role for CD147 in splenic removal of senescent red cells

90
Q

Antigen of raph blood group system

A

• antigen
• RAPH or Mer2

91
Q

reactivity is sensitive to disulfide reducing agents and most proteases except papain

92
Q

Can raph cause cause htr and hdfn

A

• no reports have described HDFN due to antiMER2

• can cause hemolytic transfusion reactions in some patients

93
Q

a monocyte monolayer assay may be helpful in determining the clinical significance of antiMER2 antibodies

94
Q

antigen is sensitive to proteases and DTT

95
Q

Clinically insignificant although shortened RBC survival has been documented in some patients

96
Q

Semaphorin proteins are implicated in cell signaling (SEMAZA)

97
Q

in hematopoietic cells, can modulate cellular immunity via effects on T cells, monocytes, and natural killer (NK)
cells

A

Semaphorin proteins

98
Q

inhibits NK cell proliferation and is a negative regulator of T cell activation

A

Semaphorin

99
Q

stimulates chemotaxis, secretion of inflammatory cytokines, and dendritic cell maturation in monocytes

A

Semaphorin proteins

100
Q

a mombrane channel capable of transporting urea and glycerolon red cella, AQP3 may play a role in molaria infection

101
Q

plays a significant role in skin differentiation and hydration through regulation of glycerol content and metabolism

102
Q

from the red cell extracellular membrane may contribute to the pathology and severity of malarial infections

A

Internalization and loss of AQP3

103
Q

in AQP3 is associated with decreased skin elasticity, poor wound healing, and eczema
• Incressed AQP3 is observed in basal cell carcinoma

A

a decrease

104
Q

can be modulated by inflammatory mediators, ultraviolet radiation, and topical glycerol

A

dermal AQP3 expression

ISBB (6 decks)

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