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**Host and Defense > Immediate Immunity: Barriers and Soluble Effectors II > Flashcards

Immediate Immunity: Barriers and Soluble Effectors II Flashcards

1
Q

In what order do the Complement pathways act?

A
  1. Alterenative Pathway
  2. Lectin Pathway
  3. Classical Pathway
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2
Q

What initiates the classical pathway?

A

C1

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3
Q

How would C1 Activate the classical pathway via interaction with IgM?

A
  1. Pentameric IgM Molecules bind to antigens on the bacterial surface and adopt the ‘staple’ form
  2. Then C1q binds to ONE bound IgM molecule
  3. Then that binding activates C1r, which cleaves and activates the serine protease C1s
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4
Q

How would C1 activate the classical pathway via interaction with IgG?

A
  1. IgG molecules bind to antigens on the bacterial surface
  2. C1q binds to AT LEAST TWO IgG molecules
  3. Then that binding activates C1r, which cleaves and activates serine protease C1s
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5
Q

Could C1 also bind to LPS to initiate the classical pathway?

A

According to a picture on his slides, Yes.

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6
Q

What is Convertase?

A

Protease that continuously cleaves it complement component

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7
Q

What does the lectin pathway target?

A

Pathogen cell surface carbohydrates

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8
Q

What initiates the lectin pathway?

A
  • Mannose Binding Lectins (MBL)

- Ficolins

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9
Q

What does MBL bind?

A

Binds with high avidity to mannose and fucose residues

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10
Q

What do Ficolins bind to ?

A

They bind olidgosaccharides containing acetylated sugars

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11
Q

Both MBLs and Ficolins contain Collagen helices and Alpha-helical coiled coils. Where are they different?

A

In their binding domain.

  • MBLs contain a Carbohydrate-recognition doman
  • Ficolins contain a Fibronectin domain
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12
Q

What do the intiators of the Lectin pathway recruit once they have bound to their targets?

A

They recruit MBL Associated Serine Proteases (MASP)

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13
Q

What are the Two types of MASPs?

A
  1. MASP-1

2. MASP-2

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14
Q

Which complement protein is cleaved by MASPs?

A

Complement protein C4

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15
Q

What are the steps in Lectin pathway activation?

A
  1. Activated MASP-2 cleaves C4 to C4a and C4b. C4b binds to the microbial surface
  2. C4b then binds C2, which is cleaved by MASP-2 to C2a and C2b, forming the C4b2a Complex
  3. C4b2a is an Active C3 Convertase cleaving C3 to C3a and C3b, which binds to the microbial surface or to the convertase itself
  4. One molecule of C4b2a can cleave up to 1000 molecules of C3 to C3b. Many C3b molecules bind to the microbial surface
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16
Q

What are the 3 routes of activation of the Alternative pathway?

A
  1. Spontaneous C3 hydrolysis
  2. Properdin-pathogen binding C3 recruitment
  3. Porteolytic c3 cleavage
    • Thrombin
    • Clotting cascade proteases
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17
Q

How is C3 spontaneously hydrolyzed?

A
  1. C3 spontaneously changes conformation to expose its thioester bond
  2. That thioester bond is unstable in aqueous environments and can react with water or another molecule
  3. At low level of constant, spontaneous C3 hydrolysis happens in the bloodstream and tissues
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18
Q

What Happens if the exposed thioester of C3 is attacked by water?

A

It becomes soluble C3b

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19
Q

What happens If the exposed thioester of C3 is attacked by an R-OH or R-NH2

A

It becomes C3b bound to a pathogen surface

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20
Q

In spontaneous hydrolysis of C3 what are the two C3 convertases?

A
  1. iC3Bb

2. C3bBb

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21
Q

What does iC3Bb do?

A

Initiates the alternative pathway

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22
Q

What does C3bBb do?

A

Drives pathogen C3b opsonization

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23
Q

How does Properdin ineract with C3bBb in spontaneous hydrolysis of C3?

A

Properdin stabilizes C3bBb on a pathogen surface

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24
Q

How does Properdin act to intitate the Alternative pathway?

A

Properdin binds to pathogen surfaces and recruits C3b

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25
Q

Complement Receptors regulate __________

A

Inflammation

26
Q

Complement receptors are expressed on ______ and _______ cells

A
  1. Innate

2. Adaptive

27
Q

Complement components induce __________ _________

A

Inflammatory responses

28
Q

Opsonized cells are targeted for destruction via ______ and ______

A
  1. Phagocytosis

2. Degranulation

29
Q

Complement drives _____ and _____

A
  1. Vasodilation

2. Extravasation

30
Q

What is Extravasation?

A

is the leakage of a fluid out of its container. In the case of inflammation, it refers to the movement of white blood cells from the capillaries to the tissues surrounding them (leukocyte extravasation), also known as diapedesis

31
Q

What complement components are considered Anaphylatoxins?

A
  1. C3a
  2. C5a
  3. C4a
32
Q

Small complement -cleavage products act on blood vessels to increase two things. What are those two things?

A
  1. Vascular permeability

2. Cell-adhesion Molecules

33
Q

What does increased permeability of blood vessels allow?

A
  1. Increased fluid leakage from blood vessels

2. Extravasation of immunoglobulin and complement molecules

34
Q

When vascular permeability and cell adhesion molecules are increased what happens to Migration of macrophages, PMNs, and lymphocytes?

A

It also increases

35
Q

What happens to the microbicidal activity of macrophages and PMNs when vascular permeability and cell adhesion molecules are increased leading to increased migration?

A

The microbicidal activity increases

36
Q

What do the anaphylatoxins activate and how?

A

Innate Immune Cells

Anaphylatoxins interact with discrete receptors on innate immune cells

37
Q

What Innate immune cells will perform Chemotaxis when activated?

A
  1. Macrophage
  2. Neutrophil
  3. Eosinophil
  4. Mast Cell
38
Q

What innate immune cells will produce cytokines when activated?

A
  1. Macrophages
39
Q

What innate immune cells will perform phagocytosis when activated?

A
  1. Macrophages

2. Neutrophils

40
Q

What innate immune cells will perform Degranulation when activated?

A
  1. Basophil
  2. Eosinophil
  3. Mast cell
  4. Neutrophil
41
Q

What Innate immune cells produce an oxidative burst when activated?

A
  1. Neutrophil
42
Q

What purpose does opsonization perform?

A

Neutralizes pathogens and targets them for phagocytosis

43
Q

T/F When only C3b binds to Cr1 it is enough to induce phagocytosis of Bacteria

44
Q

What role can C5a play in phagocytosis of bacteria?

A

It can activate macrophages to phagocytose via CR1

45
Q

T/F Complement forms a membrane attack complex

46
Q

How does the membrane attack complex form on the cells of pathogens?

A

Complement components C5-C9 assemble a complex that perforates the cell membrane

47
Q

Why does the complement membrane attack complex not destroy human cells?

A

On human cells CD59 binds to the C5b678 complex and prevents the recruitment of C9 to form the pore

48
Q

What is critical in order to prevent complement from targeting self-cells?

A

C3b and C5b removal

49
Q

What do healthy tissues express to help make sure they don’t get targeted by complement?

A

Complement regulating proteins

50
Q

What are some factors that regulate C3?

A
  1. Factor H
  2. Factor I
  3. DAF
  4. MCp
51
Q

What does DAF stand for?

A

Decay-Accelerating Factor

52
Q

What does MCP stand for?

A

Membrane Co-Factor Protein

53
Q

What do DAF and MCP do?

A

Disrupt C3 convertase C3bBb on a human cell surface

54
Q

What do Factors H and I do?

A

They inactivate C3b to give fragment iC3b

55
Q

DAF, MCP, Factors H and I can lead to ________ which causes _________

A
  1. C3 depletion

2. Pathogen susceptibility

56
Q

Slide 28 Draw out complement system overview

57
Q

What is the C3 Convertase?

58
Q

What is the C5 Convertase?

59
Q

In the classical pathway, what cleaves C4?

A

C1s ( I think)

60
Q

What is the C5 convertase in the alternative pathway?

**Host and Defense (31 decks)

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