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Applied Biochemistry > Complement System (Exam III) > Flashcards

Complement System (Exam III) Flashcards

1
Q

Component of the immune system that is genetically determines and nonspecific

A

Innate immune system

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2
Q

Elements of this system include mucous secretions, complement proteins, certain WBCs (especially neutrophils, macrophages, and dendritic cells)

A

Innate immune system

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3
Q

Component of the immune system involving lymphocytes (B cells and T cells) containing a small number of genetically encoded proteins that combine to produce an enormous variety of proteins capable of recognizing and deactivating specific antigens

A

Adaptive immune system

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4
Q

What immune system are you born with?
What immune system do you acquire?

A

Innate
Adaptive

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5
Q

First function of the complement system

A

Alter membrane pathogens and cellular debris

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6
Q

The first function of the complement system is to alter membrane pathogens and cellular debris via

A

Opsonization

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7
Q

What promotes removal of particles via complement receptors on host cells via a coating

A

Opsonization

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8
Q

Opsonization leads to the assembly of _____ on pathogens and subsequent _____

A

MAC; lysis

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9
Q

MAC

A

Membrane attack complex

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10
Q

Second function of the complement system

A

Enhance the inflammatory response

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11
Q

The complement system enhances the inflammatory response via

A

Release of anaphylatoxins that promote cell activation or migration to inflammatory site

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12
Q

Migration to inflammatory site

A

Chemotaxis

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13
Q

The complement system becomes activated in innate immunity when it senses:

A

Apoptotic cells, tissue debris or pathogens

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14
Q

Innate immune system is always functioning at:

A

A very low level

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15
Q

The body has mechanisms in place to prevent the innate immune system from:

A

Destroying all cells in our body

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16
Q

The complement system can be activated in three ways:

A
  1. C3 turnover
  2. Natural antibodies
  3. Lectins
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17
Q

Activation of the complement system by C3 turnover engages what pathway

A

The alternative pathway

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18
Q

Activation of the complement system through natural antibodies engages what pathway

A

Classical pathway

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19
Q

Activation of the complement system by binding of lectins engages what pathway

A

The lectin pathway

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20
Q

In adaptive immunity naturally antibodies are replace by:

A

Specific antibodies

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21
Q

The complement system triggers the following immune functions (3):

A
  1. Phagocytosis
  2. Inflammation
  3. Membrane attack
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22
Q

phagocytosis in the complement system occurs by:

A

Opsonizing antigens

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23
Q

has the most important opsonizing activity

A

C3B

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24
Q

occurs by chemotactically attracting macrophages and neutrophils

A

Inflammation

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25
Q

What anaphylatoxins are involved in inflammation

A

C3a C5a

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26
Q

What process ruptures the cells wall of bacteria (punching hole in it)

A

Membrane attack

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27
Q

A local response to cellular injury that is marked by capillary dilatation, leukocytic infiltration, redness, heart, and pain

A

Inflammation

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28
Q

Serves as a mechanism initiating the elimination of noxious agents and of damaged tissue

A

Inflammation

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29
Q

Wheel and flare response is characteristic of:

A

Type I allergic reaction

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30
Q

Swelling produced by the release of serum into the tissues

A

Wheal

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31
Q

Redness of the skin resulting from the dilation of blood vessels

A

Flare

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32
Q

The classic pathway is triggered by the activation of:

A

C1-complex

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33
Q

The mannose-binding (lectin) pathway is homologous to the classical pathway, but uses the opsonins:

A

Mannose-binding lectin (MBL) and ficolin

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34
Q

What opsonins does the classical pathway use

A

C1q

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35
Q

The alternative pathway is continuously activated at a ______ level

A

Low

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36
Q

The alternative pathway is continuously activated at a low level as a result of:

A

Spontaneous C3 hydrolysis

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37
Q

In the alternative pathway spontaneous C3 hydrolysis occurs as a result of:

A

Breakdown of the internal thioester bond

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38
Q

The breakdown of the the internal thioester bond in C3 is due to C3 being mildly unstable in:

A

Aqueous environment

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39
Q

Pathway that does not rely on pathogen-binding antibodies like other pathways

A

Alternative pathway

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40
Q

Pathway that responds when you have antigen:antibody complexes (on pathogen surfaces)

A

Classical pathway

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41
Q

The classical pathway involve what molecules (3)

A

C1, C4, C2

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42
Q

The C1 molecule in the classical pathway breaks down into

A

C1q, C1r, C1s

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43
Q

Pathway involving mannose-binding lectin or ficolin binding carbohydrates on pathogen surfaces

A

Lectin pathway

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44
Q

The lectin pathway involves mannose-binding lectin or ficolin binding to _____ on pathogen surfaces

A

Carbohydrates

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45
Q

What molecules does the lectin pathway involve

A

MBL/ficolin,C4, C2

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46
Q

Enzymatic activity of the MBL/ficolin complex in the lectin pathway

A

MASP-2

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47
Q

What molecules do the lectin pathway and classical pathway have in common

A

C4 and C2

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48
Q

The alternative pathway occurs on

A

Pathogen surfaces

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49
Q

The molecules involves in the alternative pathway include

A

C3, B, D

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50
Q

All three pathways converge at the production of

A

C3 convertase

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51
Q

What two pathways are pretty much identical excepting for what triggers them

A

Classical and lectin pathways

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52
Q

A molecule that cleaves different members of the complement pathways

A

C3 convertase

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53
Q

C3 convertase cleaves C3 into

A

C3a and C3b

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54
Q

After c3 convertase cleaves C3 into C3a and C3b, the C3b will bind

A

C3 convertase

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55
Q

When C3b combines with C3 convertase bind together, this leads to the cleavage of

A

C5 into C5a and C5b

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56
Q

What molecules are peptide mediators of inflamantion and phagocyte recruitment

A

C3a and c5b

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57
Q

What molecule binds to complement receptors on phagocytes and leads to the opsonization of pathogens and removal of immune complexes

A

C3b

58
Q

What molecule triggers MAC formation along with lysis of certain pathogens and cells

A

C5b

59
Q
  1. Molecule important in opsonization
  2. Molecule important in MAC formation
  3. Molecules important in inflammation
A

1- C3b
2- c5b
3- C3a & C5a

60
Q

In addition to the C3 being broken down into C3a and C3b during activation of the complement system our bodies also:

A

Constitutively hydrolyze C3 into c3a and C3b but at a very low level

61
Q

The central component of the complement system:

A

Complement fixation

62
Q

In fixation of complement what molecule tags the bacterium for destruction

A

C3b

63
Q

In fixation of the complement system what molecule recruits phagocytes and functions in inflammation

A

C3a

64
Q

Cleavage of c3 exposes a:

A

Thioester bond

65
Q

when the thioester bond is exposed on c3 this allows _____ to strongly covalently bind

A

Nucleophiles

66
Q

In the classical pathway of complement, you have antibodies coating to the surface and the ____ molecule is going to bind to that

A

C1 molecule (made of C1q, C1r, C1s)

67
Q

What subunit of the C1 molecule will cleave C4 into C4a and C4b

A

C1s

68
Q

The cleavage of c4 into c4a and c4b will induce the celaveage of:

A

C2 into C2a and C2b

69
Q

C4b and C2a together will cleave C3 into

A

C3a and C3b

70
Q

C4b + C2a together form

A

C3 convertase

71
Q

C1 is a complex of c1q, c1r and c1s. The c1q portion is composed of:

A

Six identical subunits with globular heads and long collagen-like tails

72
Q

The headlight structure of c1q function to:

A

Sit down and bind pathogen surfaces

73
Q

Once the c1q globular heads are bound to the pathogen surface, the c1r portion undergoes conformational change which results in:

A

Cleaving and activating the c1s zymogen

74
Q

C1s will bind the:

A

Receptors on the pathogen surface

75
Q

What cleaves C4 into C4a and C4b

A

Activated c1s

76
Q

When the C4b binds to C2, the C2 undergoes cleavage by ____ to form C2a and C2b

A

C1s

77
Q

After the c2 is cleaved into c2a and C2b, ___ combine with the c4b to create _____

A

C2b; c3 complement (c4bc2a)

78
Q

Because c4b2a is an activate c3 convertase it functions to cleave

A

C3 into c3a and C3B

79
Q

After c3 is cleaved by the c3 convertase it will bind either:

A

Microbial surface or the convertase itself

80
Q

One molecule of c4b2a can cleave up to _____ molecules of c3 into C3b

A

1000

81
Q

The whole process starting with the c1s binding to the microbial surface and ending with the cleavage of c3 and all the in between steps are part of the:

A

Opsonizaiton process

82
Q

When molecules get coated with _____ they are said to be opsonized

A

C3b

83
Q

In the mannose-binding lectin pathway, instead of the antibody binding event it uses:

A

Lectin binding proteins

84
Q

The Mannen-binding lectin forms a complex with ______ that resembles the complement c1 complex

A

Serine proteases

85
Q

MLB forms cluster of two to six ____ heads around a central ____ like stalk

A

Carbohydrate-binding
Collagen-like

86
Q

What are the two associated enzyme activities of the two serine proteases in mannan-binding lectin

A

MASP-1
MASP-2

87
Q

The function of the MASP-1 and MASP-2 enzymes associated with Mannan-binding lectin allows for the cleavage of:

A

C4 and C2

88
Q

Mannan-binding lectin and Ficolin both associated with:

A

MASP-1 and MASP-2

89
Q

In the mannose-binding lectin pathway, the C4b2a is a c3 convertase; it will cleave the C3 into c3a and C3B and the C3b will bind the c4b2a complex generating:

A

C5 convertase

90
Q

In the alternative pathway:

C3b is deposited by the classical pathway or lectin pathway’s:

A

C3 convertase

91
Q

In the alternative pathway:

C3b binds:

A

Factor B

92
Q

In the alternative pathway:

Bound factor B is cleaved by ________ into Ba and Bb

A

Plasma protease factor D

93
Q

In the alternative pathway:

C3bBb complex is a:

A

C3 convertase

94
Q

The alternative pathway of complement involves creating a C5 convertase that ultimately leads to the deposition of:

A

MAC complexes

95
Q

In addition to the alternative pathway, the C5 convertase can also be generated in other pathways, the key is you need to generate a ____ in order to create a convertase that will cleave C5 into C5a and C5b

A

C3b complex

96
Q

The alternative pathway is triggered by:

A

Covalent binding of C3b to pathogen or cell surface

97
Q

In the alternative pathway- what forms the pore on the membrane surface

A

C9

98
Q

The MAC complex is composed of molecules

A

C5b, C6, C7, C8, and a bunch of C9

99
Q

All three of the pathway ultimately lead up to

A

MAC complex

100
Q

What is the most direct pathway leading the the MAC complex

A

Alternative pathway

101
Q

In order for phagocytosis to follow opsonization - the phagocytic cells must contain

A

A specific receptor for the complement molecules on their surface

102
Q

If the phagocytic cells do not contain the receptors specific to the complement molecules coating the pathogen:

A

Phagocytosis will not occur

103
Q

For phagocytosis to occur what specific molecules must be present and why?

A

C5a and has to internalize it

104
Q

You can opsonize and coat the bacteria with C3b, bind them to the complement receptor on the phagocytic cell, but if _____ is not present then the bacteria will not be internalized by the phagocytic cell

A

C5a

105
Q

All of the cells in our body carry different proteins on their surfaces designed to prevent the complement pathway:

A

From attacking self cells

106
Q

Membrane protein that displaces Bb from C3b and C2b from C4b

A

Decay-accelerating factor (DAF)

107
Q

Membrane protein that promotes C3b and C4b inactivation by I

A

Membrane cofactor protein (MCP)

108
Q

DAF and MCP are both

A

Control proteins

109
Q

We have spontaneous production of ____ at low levels

A

C3b

110
Q

If you get C3b binding to autologous host membranes, it will interact with ______ which blocks the association of factor B with C3b thereby preventing the formation of ______

A

DAF
C3 convertase

111
Q

On the cell membrane, DAF causes the C3 convertase to

A

Dissociate

112
Q

MCP binding to the C3b Bb complex causes the release of the ____ portion and allows _____ to come in and bind to the C3b and cleaving it into an inactive form

A

Bb
Factor I molecule

113
Q

DAF and MCP both involve the dissociation of the Bb portion, but MCP additionally makes the C3b susceptible to:

A

Cleavage by factor I

114
Q

Factor I functions to:

A

Cleave C3b molecule into an inactive form

115
Q

Innapropriate activation of the complement pathway leads to: (2)

A

Diseased state and destroying of self cells

116
Q

Acquired disorder that results in premature death and impaired production of blood cells

A

Paroxysmal Nocturnal Hemoglobiuria

117
Q

What cells does PNH affect

A

RBCs, leukocytes and platelets

118
Q

Who does PNH affect and when does diagnosis typically occur

A

Both sexes equally
Diagnosed in young adulthood

119
Q

Paroxysmal Nocturnal Hemoglobinuria results from

A

Deficiency of the DAF protein

120
Q

Paroxysmal nocturnal hemoglobinuria gets its named based on it occuring mainly at:

A

Night

121
Q

In PNH the deficiency of DAF protein:

A

Results in destruction of self cells

122
Q

Results from chronic uncontrolled activation of the complement system

A

Atypical hemolytic uremic syndrome

123
Q

Disease in which multiple blood clothes form throughout the body in small blood vessels, which can lead to stroke, heart attack, kidney failure and death

A

Atypical hemolytic uremic syndrome

124
Q

Atypical hemolytic uremic syndrome is due to

A

Mutations in factor H, factor I, or membrane cofactor protein

125
Q

The most common functional defect in atypical hemolytic uremic syndrome and age-related macular degeneration is:

A

Reduced cofactor activity (MCP or factor H) for C3b

126
Q

Atypical hemolytic uremic syndrome is a very _____ disease in terms of which protein is affected which also determines:

A

Heterogeneous
The severity of the disease

127
Q

In Atypical hemolytic uremic syndrome, the post commonly affected factor causing the disease is

A

Factor H

128
Q

In normal conditions MCP or factor H will bind to C3b when C3b is created, this is when factor I comes in and cleaves C3b into an inactive form. If you don’t have a functional MCP or factor H:

A

Factor I will be unable to bind

129
Q

If there is any spontaneous creation of C3b from C3 convertase or the hydrolysis that occurs naturally the molecules of our defense mechanism are there to prevent:

A

Initiation of the complement cascade which leads to cell death

130
Q

Disease characterized by recurrent attacks of severe swelling

A

Hereditary angioedema

131
Q

Angioedema caused by mutations in the gene that makes the C1 inhibitor

A

Type I & Type II

132
Q

Hereditary angioedema caused by deficiency of C1

A

Type I

133
Q

Hereditary angioedema caused by atypical C1 protein that is less capable of suppressing acitvation of complement system

A

Type II

134
Q

Hereditary angioedema associated with mutations in Factor XIII gene

A

Type III

135
Q

Factor-XII gets cleaved into Factor-XIIa also known as

A

Plasmin

136
Q

Factor-XIIa (Plasmin) function to cleave:

A

Prekallikrein into Kallikrein

137
Q

Factor-XIIa also functions in the conversion of the _____ pathway of the clotting cascade

A

Common

138
Q

Kallekrein convertes a high-molecular-weight Kininogen into

A

Bradykinin

139
Q

Bradykinin plays a role in (3)

A

1- vasodilation
2- smooth muscle contraction
3- edema

140
Q

The classic pathways works through:

A

Antigen-antibody complexes and C1

141
Q

The lectin pathway and alternative pathway function within the ____ immune system, whereas the classical pathway functions with _____ immune system

A

Lectin & alternative = innate immune system
Classical = both innate and adaptive immune system

Applied Biochemistry (18 decks)

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