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IMSE 311 > Complement > Flashcards

Complement Flashcards

1
Q

Alteration of a complement (protein) in such a way that it can proceed to interact with the next component in the pathway (cascade)

A

Complement Activation

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2
Q

Utilization of complement components by the antigen-antibody complex.

A

Complement Fixation

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3
Q

Complements that have enzymatic activities

A

C1, C2, C3, C4

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4
Q

Complements that don’t have enzymatic activity

A

C5, C6, C7, C8, C9

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5
Q

Complement’s order of activation

A

C1, 4, 2, 3, 5, 6, 7, 8, 9

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6
Q

Complement’s order of discovery

A

C1, 2, 3, 4, 5, 6, 7, 8, 9

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7
Q

The dilution of a serum sample which can lyse a predetermined proportion of a sheep erythrocyte (srbc) suspension coated with anti-SRBC antibody.

A

Hemolytic Units

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8
Q

Denaturation (usually by heat) of one of the early components in -activation pathway resulting in the destruction of C-hemolytic activity.

A

Complement Inactivation

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9
Q
  • Soluble and cell bounded protein
  • Heat-labile proteins
  • Predominantly inactive molecule
  • All are produced on Liver
A

Characteristics of Complement

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10
Q

Small soluble proteins that regulate the immune system, orchestrating both innate immunity and the adaptive response to infection

A

Complement

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11
Q

Who coined the Complement System?

A

Paul Ehrlich

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12
Q

Who explain the nature of complement?

A

Jules Bordet

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13
Q

Where do Factor D come from?

A

Adipose Tissue

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14
Q

Where do C1 Components come from?

A

Intestinal Epithelial Cell

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15
Q

Other source come from?

A

Macrophage, Monocyte

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16
Q

Thermolabile in

A

56°C for 30 mins

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17
Q

It regains activity at what temperature?

A

7 - 37°C

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18
Q

It lost activity in ___ at ___?

A

3 - 4 days at Refrigerator temperature

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19
Q

It deteriorates within ___ at ___?

A

1 - 2 days at room temperature

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20
Q

It reacts best at ___ in ___?

A

pH 7.2 - 7.4 in 30 - 37°C

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21
Q

(True or False)

It has Calcium and Magnesium

A

True

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22
Q

(True or False)

It is bound to all antigen-antibody complexes

A

True

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23
Q

(True or False)

It CANNOT be activated by non-serologic reactions

A

False

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24
Q

Complement is preserved BEST by ____?

A

Lyophilization

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25
Q

What are the 3 phase for each of the main pathway?

A
  1. Initiation
  2. Amplification
  3. Membrane Attack Complex (MAC)
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26
Q

Its activation proteins are C1qrs, C2, C3, and C4. What pathway is this?

A

Classical pathway

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27
Q

Its activation proteins are MBP, MASP, MASP2. What pathway is this?

A

Lectin pathway

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28
Q

Its activation proteins are C3, Factor B, and D Properdin. What pathway is this?

A

Alternative pathway

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29
Q

It has C5, C6, C7, C8, and C9. What pathway is this?

A

Lytic pathway

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30
Q

Its Stimulus has Antigen-Antibody complexes, CRP, E.coli, Mycoplasma, Protozoa

A

Classical

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31
Q

Its stimulus is Lipopolysaccharide, Fungal Cell [zymosan], Yeast, Parasites [trypanosmoes, tumor cell lines, Cobra venom factor

A

Alternative

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32
Q

Its stimulus is mannose and several other sugars found primarily on bacteria, some yeasts, viruses, and several parasites

A

Lectin

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33
Q

A pathway that is not calcium-dependent cause it has magnesium

A

Alternative

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34
Q

These pathways are calcium dependent

A

Classical and Lectin

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35
Q

What are the common Activation unit of the 3 pathways?

A

C3 convertase and C5 convertase

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36
Q

Membrane Attack Complex (MAC)

A

C5, C6, C7, C8, C9

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37
Q

What are the 3 pathways of complement activation?

A
  1. Classical pathway
  2. Alternative pathway
  3. Lectin pathway
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38
Q

It bind to fc portion of IgG (CH2) & IgM (CH3) ; B binds to C3b to form C3 convertase

A

C1q

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39
Q

Cleaves to C4 & C2 ; D - Cleaves to factor B into Bb in the presence of C3 and Mg ions

A

C1s

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40
Q

This is the key component of each pathway ; Properdin - stabilize C3 convertase

A

C3

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41
Q

It initiates MAC

42
Q

Stabilizes and binds C5b ; Lectin pathway

42
Q

It has affinity to lipid component / Allows insertion of complex ; MBL - binds to mannose

43
Q

Expose hydrophobic region [pore formation] ; MASP 2 - acts like C1s

44
Q

Accelerates cell lysis ; MASP 1,2,3 - bind to form an activated C1 like complex

45
Q

Anaphylaxis; cause increased vascular permeability, contraction of smooth muscle, and release of histamine from basophils (induces)

A

C3a, C4a, C5a

46
Q

An opsonin

47
Q

Opsonization

A

C3b, C4b, C5b

48
Q

membrane attack complex

A

C5b, C6, C7, C8, C9

49
Q

Chemotaxin & Anaphylaxin –> Attacks WBC to inflammation

50
Q

Analogous/same to C1r and C1s

51
Q

These two acts the same

A

C1q and MBL

52
Q

(True or False)

C1q is analogous to MBL

53
Q

What is the end result of the complement pathway?

A

Cell lysis (suicidal bomb)

54
Q

Largest/biggest than other C1

55
Q
  • First to be studied
  • Initiated by Ag-Ab complex
  • IgM>IgG3>IgG1>IgG2
A

Classical Pathway

56
Q

It can be seen in the cell wall of bacteria, virus, and some parasites

57
Q

In IgM it needs 1, but in IgG it needs how many?

A

2 adjacent molecules

58
Q

Cause basophil/mast cells degranulation and smooth muscle contraction

A

Anaphylatoxin (C4a, C3a, C5a)

59
Q

Promotes phagocytosis

A

Opsonins (C3b)

60
Q

Promotes diapedesis

A

Chemotactic factor (C5a)

61
Q

Recognition

62
Q

Trimolecular structure of C1q, C1r, C1s is stabilized by ____?

A

Calcium ions

63
Q

Classical pathway activates

A

C4, C2, C3

64
Q

(True or False)

Alternative pathway bypasses C1, C4, and C2,

64
Q
  • Aggregates of IgA
  • Yeast cell wall or Zymosan
  • Lipopolysaccharides
  • CVF: Cobra venom factor
A

Alternative/ alternate/ properdin pathway

65
Q

(True or False)

Alternative pathway is activated at a slow rate by water and plasma enzymes

66
Q

Alternative pathway starts/begins activation at ___?

67
Q
  • MBL: Mannose-Binding Lectin
  • Attaches to mannose or similar sugar in cell walls or outer membranes of microorganisms
  • Cleaves C4 and C2 (formation of C3 convertase); Proceed as classical
A

Lectin pathway

68
Q
  • Opsonization; phagocyte activation
  • Phagocytosis
  • Factor H and I
A

C3b and its products

68
Q
  • Basophil and mast cell degranulation; smooth muscle contraction
  • Anaphylaxis
  • Carboxypeptidase B (C3a-INA)
A

C3a, C4a (Anaphylatoxin)

69
Q
  • Accumulation of body fluid
  • Edema
  • C1-INH
A

C2b (Prokinin)

70
Q
  • Basophil and mast cell degranulation; smooth muscle contraction
  • Anaphylaxis
  • C3a-INA
A

C5a (Anaphylatoxin; Chemotactic factor

71
Q
  • Chemotaxis; attachment to other cell membbrane
  • Inflammatory lysis of by stander cells
  • Protein S (MAC)
72
Q

Dissociates C1r and C1s from C1q

A

C1 inhibitor

73
Q

Cofactor with I to inactivae C3B; prevents binding of B to C3b

74
Q

Cleaves C3b and Cb

75
Q

Accelerates dissociation of C3 convertase

A

Decay accelerating Fcator / CD55

76
Q

Acts as a cofactor with I to inactivate C4b

A

C4-binding protein / membrane cofactor protein / CD46

77
Q

Acts as a cofactor with I and binds C3b

A

CR1 / CD35

78
Q

Inhibits MAC through binding with CD8 to prevent insertion of CD9

A

Membrane inhibitor of reactive lysis MIRL / CD59

79
Q
  • Inhibits MASP-2, C1r, C1s
  • From Liver Macrophage
A

C1 Inhibitor

79
Q

Prevents attachment of C5b67 complex to cell membrane

A

S protein / vitronectin

80
Q
  • Inhibits C4b
  • Acts with DAF, CR1, MCP
81
Q
  • Binds with C3b
  • Blood cells
  • CD35
A

Complement Receptor 1

82
Q
  • Cofactor to C4b, C3b, Factor B
  • CD46
A

Membrane Cofactor Protein

83
Q
  • Binds to C4b, C3B and dissolves C2a
  • From Epithelial cell, endothelial cell, fibroblasts
  • CD55
A

Decay-accelerating Factor

84
Q

Lupus-like syndrome; recurrent infections

A

C1 (1q,r,s) deficiency

85
Q
  • Prevent insertion of C9
  • Blood cell
  • CD59
A

Membrane inhibiting reactive lysis

85
Q
  • Prevent the binding of Factor B and C3b
  • 100x affinity to C3b
86
Q

Prevent from binding to cell membrane

A

S protein or Vitronectin

87
Q

Lupus-like syndrome, recurrent infections, artherosclerosis
Most common complement deficiency

A

C2 deficiency

88
Q

Glomerulonephritis
Most severe complement deficiency
Most commonly measured

A

C3 deficiency

89
Q

Lupus-like syndrome

A

C4 deficiency

90
Q

Neisseria infections

A

C5 - C8, Properdin deficiency

91
Q

No known disease association

A

C9 deficiency

92
Q

Hereditary angioedema

A

C1-INH deficiency

93
Q

Paroxysmal nocturnal hemoglobinuria

A

DAF, MIRLs deficiency

94
Q

Recurrent pyogenic infections

A

Factor H or I deficiency

95
Q

Pneumococcal diseases, sepsis, Neisseria infection

A

MBL deficiency

96
Q

Pneumococcal infections

97
Q

Most important and if you are deficient in this it will cause severe problems

IMSE 311 (4 decks)

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