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Complement Flashcards

1
Q

Why is complement so named

A

It was identified as a heat-labile component of the serum that complemented the antibacterial properties of Ab

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2
Q

Are complement molecules always free

A

Some are soluble and some are membrane associated

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3
Q

In general, is fragment b bigger or smaller

A

Bigger

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4
Q

What are the 3 major functions of complement

Name some additional roles

A

Activation of inflammation
Opsonisation
Lysis of target cells

Clearance of immune complexes and apoptotic cells, stimulating adaptive responses

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5
Q

Which unusual bond in C3 is v important

A

Internal thioester bond

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6
Q

What happens when C3 is cleaved into C3a and C3b

What does this allow

A

The thioester bond in C3b is exposed and can react with hydroxyl or amino groups

Covalent linking of C3b to pathogen surface, opsonising the pathogen for phagocytosis
Also stimulates generation of more C3b

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7
Q

What does C3a do

A

It is an anaphylotoxin that stimulates local inflammation

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8
Q

Probably the most important function of complement is to facilitate the uptake and killing of pathogen is by phagocytic cells. How is this controlled?

A

Complement Receptors (CRs) that recognise proteolytic derivatives of C3

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9
Q

Which CRs are particularly important for the phagocytosis of complement tagged bacteria?

A

CR1 and CR3

CR1 binds directly to C3b

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10
Q

In the absence of an antibody, macrophages require an additional signal to C3b. What is this signal?

A

C5a and C5a receptor

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11
Q

Which blood cell highly expresses CR1

What does this mean

A

erythrocytes

It can bind C3b attached to the antibody/antigen immune complexes so they can be removed from the blood for clearance in the liver

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12
Q

What causes immune-complex disease

A

Low CR1 levels

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13
Q

What are the 3 major pathways that lead to activation of complement of

What order do they act in

A

1st - Alternative pathway
2nd - Lectin pathway
3rd- Classical pathway

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14
Q

What does the alternative pathway in complement rely on

A

Spontaneous conformational changes in C3 that expose the internal thioester group

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15
Q

What does the spontaneous exposure of the internal Thioester group in C3 lead to an aqueous environment?

What does this allow

A

Generation of C3H2O

Association with factor B

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16
Q

What can happen when C3(H2O) has associated with factor B?

What happens next?

A

It is susceptible to cleavage by the factor D

The large fragment (Bb) remains associated with C3(H2O) —-> C3(H2O)Bb

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17
Q

What type of enzyme is a factor D

A

Serine protease

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18
Q

What does C3(H2O)Bb do

What is another name for this molecule

What is its role

A

It is a protease that can cleave C3 into C3a and C3b

Aqueous/ fluid phase C3 convertase

To produce enough C3b so that some will attach to the activating surface of the pathogen

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19
Q

True or false

Microbial services are by default “activating”

A

True

They generally lack regulatory mechanisms to deactivate complement

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20
Q

What happens to C3B when attached to a surface in the alternative pathway

What is this called

A

It combined factor B and generate surface bound C3bBb

Alternative pathway C3 convertase

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21
Q

What is Alternative pathway C3 convertase able to do

What do these molecules do

A

Generate more membrane-bound C3b and soluble C3a

C3b acts as an opsonin and provides a positive feedback loop to form more C3bBb

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22
Q

What is alternative C5 convertase?

A

Instead of binding to a service, cleaved C3b can remain attached to C3bBb to form C3b2Bb

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23
Q

What does C3b2Bb do?

What is the point?

A

Cleaves C5 into C5a and C5b (C3b2Bb = Alternative C5 convertase)

To form the membrane attack complex

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24
Q

What happens in the alternative pathway when C5b is formed

A

C6 and C7 bind to C5b, allowing C7 to insert into the lipid membrane

C8 binds to C5b67 - this allows insertion into the membrane and subsequent polymerisation of C9 subunits to form a membrane pore

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25
Did alternative pathway is effective against which pathogens
Gram negative bacteria and enveloped viruses
26
How is the Lectin pathway activated
Mannose binding lectin (MBL) and M-,H-, or L-ficolin
27
What kind of molecule is MBL What is it comprised of
A ‘collectin’ and a PRR Collagen and Lectin domains, hence COLL- LECTIN
28
MBL is a PRR. what does it bind
Close knit a raise of mannose and fructose residues that are found on microbial services of bacteria, yeast, fungi and viruses but not the host
29
Are MBL molecules membrane bound What are they associated with
No They circulate in plasma in association with 2 serine proteases
30
What are the 2 MBL associated serine proteases When do they activate What do they do
MBL-associated Serine Protease (MASP) 1 and 2 Upon binding the pathogen surface Cleave C4 and C2
31
Why is C4 similar to C3
Both have an internal thioester bond and C4b can attach to the pathogen surface
32
What happens when C4b binds to the pathogen surface
It is joined by C2a to form C4bC2a
33
What is another name for C4bC2a
The Classical C3 Convertase
34
True or false | Complement components usually act sequentially
This is mostly true of C1-9 with the exception of C4
35
What is unusual about C2
C2a > C2b
36
When can the Classical Pathway be activated
If the surface of the pathogen can be recognised by antibody or C-reactive protein
37
How does the binding of antibody to a surface help the classical pathway
It exposes a binding site for C1q present in the Fc region of some antibody isotypes
38
What happens when a molecule of C1q binds to several Fc regions?
The conformational change activates the C1r and C1s subunits
39
What does C1s do What happens to C1 next
It is able to cleave C4 to expose the thioester group which can covalently attach C4b to pathogen surface Activated C1 associates with and cleaves C2, allowing C4bC2a
40
What is C4bC2a What does it do
The Classical C3 Convertase Cleaves C3 to allow C3b to bind to microbial surface This then uses the alternative pathway amplification loop by binding to factor B to generate C3bBb
41
What is a classical pathway C5 convertase
C4bC2aC3b Generated when C4bC2a (classical C3 Convertase) associates with C3b
42
How long is the half life of C3bBb Is this representative for the life span of complement components
~90 secs Yes they are relatively unstable and quickly lose activity
43
Name a positive regulator of the alternative pathway How many positive regulators are known
Properdin (Factor P) Only 1
44
What does Factor P do
Stabilises C3bBb and increases activity 5-10 fold Stabilises 5 convertase complex assisting in MAC complex formation
45
What is Factor I
A soluble constitutively active serine protease
46
What does Factor I degrade Does it do this alone?
C3b and C4b It requires cofactors such as MCP and Factor H
47
What is MCP Where is it expressed What does it do
Membrane Cofactors Protein Host cell membranes Induces dissociation of C4bC2a and C3bBb, and cleavage of C3b and C4b by Factor I
48
True or false | MCP has decay accelerating capacity but not factor I cofactor activity
False | It has both decay accelerating capacity and factor I cofactor activity
49
Which Complement Receptor acts in a similar way to MCP
CR1
50
What is the main control factor responsible for regulating complement activation in solution
Factor H
51
What is factor H
A soluble cofactor for Factor I that attaches sialic acid present on host membranes
52
What does Factor H attach to Where is this found
Sialic acid Host membranes but is absent in most bacteria
53
What does Factor H induce
Dissociation of C3bBb complexes and makes C3b susceptible to cleavage by Factor I
54
What is DAF Where is it found What does it do
Decay accelerating factor On the surface of host cells Dissociates the classical (C4bC2a) and alternative (C3bBb) C3 convertases
55
What is protectin
A host cell surface protein that binds the MAC intermediate C5b678 and prevents its insertion into membranes Also interacts with C9 and prevents its recruitment to the MAC complex
56
How do early components of complement pathways facilitate clearance of soluble immune complexes? Components of Which pathway is responsible for this
Coating them with C4b and C3b Classical pathway
57
Who suffers from immune complex disease
Individuals with defects in C1-4 as they cannot clear immune complexes from the blood
58
What does defects in C3 result in Why is this What else can lead to the same result
Susceptibility to pyogenic infections (ie pus forming infections such as staphylococcus and streptococcus) It is an important opsonin assisting in phagocytosis of bacteria Defects in activating C3
59
What is the most effective defence against Neisseria Who would suffer from recurrent Neisseria infections
Complement mediated lysis Individuals with deficiencies in membrane attack components C5-9
60
Control of which kind of bacteria relies heavily on opsonisation
Encapsulated bacteria
61
Defects in generation of which complement components result in susceptibility pyogenic infection
C3b | Factor D and properdin
62
What can lead to C3 depletion What does this result in
Uncontrolled alternative pathway activation Factor I and Factor H deficiency And leads to susceptibility to pyogenic infection
63
Why does a reduced GPI synthesis lead to reduced DAF and protectin on RBCs What does this cause
DAF and protectin are GPI-anchored proteins Paroxysmal Nocturnal Hemoglobinuria
64
What is PHN?
Paroxysmal Nocturnal Hemoglobinuria Complement mediated lysis of RBCs because of reduced expression of DAF and protectin on erythrocytes
65
Name 4 complement evasion strategies
Interference of antibody-complement interactions Binding and inactivation of complement components Destruction of complement components by proteases Mimicry of inhibitory regulators or recruitment of host inhibitors
66
Which pathogen is a good example of complement evasion
Staphylococcus aureus
67
How does staphylococcus aureus avoid complement (6)
The cell wall is protected by a polysaccharide capsule to prevent opsonisation Secretes proteins that bind or degrade C3 Staphylococcal Protein A binds the Fc region of IgG blocking complement recruitment Clumping factor A recruits Factor I to the bacterial surface Chemotaxis Inhibitory Protein blocks C5a chemotactic receptor on neutrophils Neutrophil extravasation is interfered with
68
What happens if C3 Convertase does manage to assemble at the site of staphylococcus aureus infection
C3 Convertase is bound and inactivated by Staphylococcus Complement Inhibitor (SCIN) preventing generation of opsonins (eg C3b)

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