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biochemistry (cole) > Lecture 24 Complement System > Flashcards

Lecture 24 Complement System Flashcards

1
Q

Innate immune system

A

The component of the immune system in animals that is genetically determined and is nonspecific as distinguished from the adaptive immune system.

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2
Q

Elements of innate immune system

A
  • Mucous secretions
  • Complement proteins
  • Certain White blood cells
  • Especially neutrophils
  • Macrophages
  • Dendritic cells (medical dictionary)
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3
Q

Adaptive Immune System

A
  • The component of the vertebrate immune system involving lymphocytes (B cells and T cells) containing a small number genetically encoded proteins that combine to produce to an enormous variety of proteins capable of recognizing and deactivating specific antigens
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4
Q

Complement Functions

A
  1. Alters the membrane of pathogens and cellular debris

2. Enhance the inflammatory response

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5
Q

Membrane Perturbation

A
  • Alters membrane of pathogens and cellular debris
  • Opsonization
  • Opsonization leads to assembly of the membrane attack complex on pathogens and subsequent lysis
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6
Q

Opsonization

A

coating promotes removal of particles via complement receptors on host cells

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7
Q

Inflammatory response

A

-Release of anaphylatozins that promote cell activation (e.g. mast cell degranulation) migration
OR
- Migration to an inflammatory site (chemotaxis)

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8
Q

What do mast cells produce?

A

Histamine

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9
Q

What are the three types of complement system activation?

A
  1. C3 turnover (Alternative Pathway)
  2. Natural ABs (Classical pathway)
  3. Lectins (Lectin Pathway)
    - Three mechanisms are independent of a prior adaptive immune response
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10
Q

Complement activation

A
  • innate immunity

- complement system becomes activated on a target such as apoptotic cells, tissue debris or pathogens

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11
Q

C3 Turnover

A
  • spontaneously activated

- Engages alternative pathway

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12
Q

Binding of the target of naturally occurring antibodies engages what pathway?

A

Classical pathway

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13
Q

Lectin pathway

A

binding of lectins to carbohydrates on the target

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14
Q

Complement triggers the following immune functions

A
  • Phagocytosis
  • Inflammation
  • Membrane attack
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15
Q

Phagocytosis

A
  • by opsonizing antigens

- C3b has most important opsonizing activity

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16
Q

Opsonizing

A

coating invading organism with proteins that body will recognize and destroy

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17
Q

Inflammation

A
  • by chemotactically attracting marcrophages and neutrophils (anaphylatoxins C3a and C5a)
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18
Q

Membrane attack

A

by rupturing cell wall of bacteria

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19
Q

Inflammation

A

a local response to a cellular injury that is marked by capillary dilatation, leukocytic infiltration, redness, heat, and pain and that serves as a mechanism initiating the elimination of noxious agents and of damaged tissue (medical dictionary)

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20
Q

Type 1 allergic reaction

A
  • Wheal and flare
  • Swelling is porduced by the release of serum into the tissues (wheal) and
  • redness of skin resulting from the dilation of blood vessels (flare)
21
Q

What triggers the classic pathway?

A

Activation of C1 complex

22
Q

What does the mannose binding lectin pathway use instead of C1q?

A
  • Opsonins
  • Mannose binding lectin
  • Ficolin
23
Q

How is the alternative pathway continuously activated at a low level?

A

As a result of spontaneous C3 hydrolysis due to the breakdown of the internal thioester bond
(the alternative pathway does not rely on pathogen-binding antibodies like the other pathways)

24
Q

Where do the Classical pathway, Lectin pathway, and alternative pathway converge?

A

C3 convertase

25
Q

How does the C1 complex proceed with opsonizing the pathogen surface?

A
  1. C1 s cleaves C4 into C4 a and b and C2 into C2a and C2n
  2. C4b and C2a bind forming the C4b2a complex
  3. C4b2a is an active convertase of C3
  4. C4b2a cleaves C3 into C3a and C3b (can cleaves 1000s of C3 molecules)
  5. C3b binds and coats bacterial surface
26
Q

What is C3a’s role in the complement system?

A
  • it recruits phagocytes
27
Q

What are the two methods that C3b can be attack the bacteria after its thioester bond is exposed?

A
  • Attack by H20 (soluble)

- Attack by R-HO or R-NH2

28
Q

What does the mannose binding lectin form a complex with?

A

Serine proteases

29
Q

Ficolins

A
  • have a different binding domain than the Mannose binding lectin
30
Q

What complex does the mannose binding lectin pathway form to convert C3 to C3b and a?

A

C4b2a

31
Q

Where does the alternative start?

A

Once C3b is already bound to pathogen surface

32
Q

What are the steps of the alternative pathway?

A
  1. C3b bound to surface (from classical or LBP)
  2. C3b binds factor B
  3. Factor B is cleaved by factor D
  4. C3bBb complex is formed and is the C3 convertase
33
Q

`What pathway provides the C5 convertase?

A

Alternative

34
Q

How is the C3b2 formed?

A

another 3b molecule binds to it after being cleaved.

35
Q

What are the steps of the mac attack?

A
  1. C5b binds to C6 and C7
  2. C5b67 complex binds to membrane
  3. C8 binds to complex and inserts into membrane
  4. C9 molecules bind to the complex and polymerize
  5. 10-16 molecules of c9 bind to form a pore in the membrane
36
Q

How do phagocytic cells bind to pathogen?

A

They have receptors that recognize the opsonization of C3b

37
Q

What needs to be present to internalize the bacterial cell?

A

C5A

38
Q

What does C5A do?

A

Activates macrophages to phagocytose/internalize

39
Q

Where are the factors that regulate the complement system?

A

The cell membrane of normal cells

-The factors prevent mac attacks

40
Q

How is the complement system regulated?

A
  • Complement activation is regulated by a series of proteins that serve to protect host cells form accidental damage
41
Q

DAF Decay Accelerating factor

A
  • Blocks the association of factor B with C3b

- Accelerates the dissociation of Bb from C3b in C3 convertase which stops the production of additional C3b

42
Q

MCP

A

dissociates C3 convertases at human cell surfaces and makes them susceptible to cleavage by factor I

43
Q

Hereditary angiodema

A

spontaneous random huge swelling

44
Q

What does MCP do?

A

Binds to C3b allowing factor I to cleave it.

45
Q

C3a, C5a

A
  • Peptide mediators of inflammation

- Phagocyte recruitment

46
Q

C3b

A
  • Binds to complement receptors on phagocytes
  • Opsonization of pathogens
  • Removal of immune complexes
47
Q

Terminal complement components

C5b, C6, C7, C8, C9

A
  • membrane-attack complex

- Lysis of certain pathogens and cells

48
Q

Eculizumab

A
  • inhibits C5 convertase

- Tested for HUS and paroxysmal nocturnal haemoglobinuria

biochemistry (cole) (25 decks)

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