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Host Defense Exam 1 > Complement > Flashcards

Complement Flashcards

1
Q

What are the effects of complement activation?

A
  • recruit phagocytes
  • killing the pathogen through lysis (MAC)
  • opsonization and antigen clearance
  • generate an inflammatory response
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2
Q

Define complement activation.

A

Complement components create complexes on the surface of pathogenic antigens to facilitate an immune response. Soluble fragments are also produce that are important. There are 3 pathways.

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3
Q

What are the complement activation pathways and their stimuli?

A
  1. Classical pathway = antibody binds to antigen
  2. Lectin pathway = MBL/ficolin binds to mannose/oligosaccharides
  3. Alternative pathway = components bind directly to pathogen surface
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4
Q

Describe the sequential events for C1qrs activation.

A
  1. antibody binds to antigen, opening up a site on the Fc for C1q
  2. 2 C1q globular heads must simultaneously bind to the antibody
  3. Once bound, C1r cleaves C1s => C1s is active
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5
Q

Describe the sequential events for MASP activation.

A
  1. Mannin Binding Lectin (MBL) or ficolin bind to mannose/oligosaccharides on pathogen surface
  2. MBLs and ficolin have 2 associated serine proteases (MASP1/MASP2)
  3. MASP1 cleaves MASP2 => MASP2 is now active
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6
Q

Describe the sequential events that lead to MAC in classic/lectin pathway

A
  1. Activation of C1s and MASP2 (see previous cards)
  2. C1s/MASP2 cleave C4 => C4a and C4b
  3. C4b binds to the pathogen surface
  4. C2 binds to C4b
  5. C1s/MASP2 cleave C2 => C2b and C4b2a
  6. C4b2a is a C3 convertase => cleave C3 => C3a and C4b2a3b
  7. C4b2a3b is a C5 convertase => cleaves C5 => C5a and C5b
  8. C5a is a soluble inflammatory mediator
  9. C5b complexes with C6, 7, 8, and 9 to create the MAC
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7
Q

What is important about C3 convertase?

A

major point of amplification

- 1 C3 convertase can cleave 1000s of C3s

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8
Q

What complex is a C5 convertase?

A
  • C4b2a3b

- C3bBb3b

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9
Q

What complex is a C3 convertase?

A
  • C4b2a
  • C3(H2O)Bb
  • C3bBb
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10
Q

Describe the sequential events that lead to MAC formation by the alternative pathway.

A
  1. C3 is hydrolyzed to form C3(H2O)
  2. C3(H2O) binds to Factor B
  3. Factor D cleaves C3(H2O)-B => Ba and C3(H2O)Bb
  4. C3(H2O)Bb is a C3 convertase => C3a and C3b
  5. Most C3b is degraded, but some attaches to the pathogen surface
  6. Factor B binds to C3b on the surface
  7. Factor D cleaves Factor B => Ba and C3bBb
  8. Properdin (Factor P) binds to C3bBb and stabilizes it
  9. C3bBb is a C3 convertase => C3a and C3bBb3b
  10. C3bBb3b is a C5 convertase => C5a and C5b
  11. C5b complexes with C6, 7, 8, 9 to form MAC
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11
Q

What effects do soluble components C3a and C5a have?

A
  • recruit phagocytes
  • promote inflammation
  • C5a also stimulates phagocytosis
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12
Q

What is the receptor for C3b?

A

CR1 found on phagocytes

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13
Q

What are the functions of C4b2a3b?

A
  • C5 convertase
  • powerful opsonin
  • enhances antigen uptake
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14
Q

How does complement activation lead to cell lysis?

A
  • formation of MAC
  • pore disrupts homeostasis
  • causes lysis
  • also works on viruses
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15
Q

How does complement activation lead to opsonization?

A
  • phagocytic leukocytes (neutrophils and macrophages) express CR1
  • CR1 binds to C3b or C4b on an antigen and enhances adherence and ingestion
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16
Q

How does complement activation lead to antigen clearance?

A
  • antigen:antibody complexes bind to CR1 (via C3b) on circulating RBCs
  • RBCs go to spleen or liver, where resident phagocytes remove the complex from their surface
17
Q

How does complement activation lead to inflammation?

A

Chemotaxis
- C5a attracts phagocytes via a C5a gradient in activation areas

Vascular Changes

  • C3a, C4a, C5a bind to receptors on mast cells and basophils
  • cause histamine release
  • increase vascular permeability => fluid leakage and immune cell recruitment
18
Q

What are anaphylatoxins?

A

C3a, C4a, C5a

cause increase in vascular permeability

19
Q

Describe inhibition of C1.

A

via C1 INH

- dissociates C1r and C1s from C1qrs

20
Q

Describe inhibition of C3 convertase.

A

inhibition of C3 convertase causes dissociation of C4b2a

  • decay-accelerating factor (DAF)
  • C4-binding protein (C4BP)
  • complement receptor 1 (CR1)
  • membrane cofactor protein (MCP)
  • Factor I
21
Q

Describe inhibition of C5 convertase.

A

inhibition of C5 convertase causes dissociation of C4b2a3b

  • Factor I
  • Factor H
  • complement receptor 1 (CR1)
22
Q

What inhibits both C3 and C5 convertase?

A
  • Factor I

- CR1

23
Q

How is MAC formation regulated?

A

CD59 prevents complexing with C9

24
Q

What do deficiencies in early complement components of the classical pathway lead to?

A
  • deficient in C1, 2, 4

- immune complex disease

25
Q

What do deficiencies in early complement components of the lectin pathway lead to?

A
  • deficient in MBL, ficolin, MASP1/MASP2, C2, C4

- bacterial infections

26
Q

What do deficiencies in early complement components of the alternative pathway lead to?

A
  • deficient in factor B and factor D

- pyogenic bacterial infection, Nisseria, NO immune complex disease

27
Q

What does a C3 deficiency lead to?

A
  • pyogenic bacterial infections
  • Nisseria
  • some immune complex disease
28
Q

What do deficiencies in C5-9 lead to?

A

Nisseria infection only

29
Q

Describe Hereditary Angioneurotic Edema.

A
  • C1 INH deficiency
  • overactive C1
  • fluid accumulation, epiglottal swelling
30
Q

Describe Paroxysmal Nocturnal Hemoglobinurea.

A
  • impaired CD59
  • increased MAC formation
  • RBC lysis

Host Defense Exam 1 (12 decks)

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