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Immunology > Week 1 - Complement > Flashcards

Week 1 - Complement Flashcards

1
Q

What are extracellular pathogens?

A
  1. Replicate outside of the cell
  2. Susceptible to secreted molecules of the immune system
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2
Q

What are examples of extracellular pathogens?

A

Bacteria, viruses, parasites, fungi

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3
Q

What are intracellular pathogens?

A
  1. Replicate within the cell
  2. Immune system must kill the cells that contain the intracellular pathogen
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4
Q

What are examples of intracellular pathogens?

A

Viruses and some bacteria

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5
Q

What happens when a virus is released from the cell?

A

Suspecitible to soluble proteins of the immune system

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6
Q

What happens when a pathogen breaches anatomical barriers?

A

Soluble molecules in extracellular fluid, blood, and epithelial secretions kill or weaken pathogen

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7
Q

What are examples of soluble molecules that weaken pathogen?

A
  1. Antimicrobial enzymes
  2. Antimicrobial peptides
  3. Complement system
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8
Q

What are antimicrobial enzymes?

A

Lysozyme and phospholipase found in tears and saliva that digest peptidoglycan in bacterial cell walls

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9
Q

What are antimicrobial peptides?

A

Defensins lyse bacterial cell wall and act as chemoattractants for phagocytes

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10
Q

What is a complement system?

A
  1. Enzymes and proteins that target pathogen for lysis or phagocytosis by the innate immune cells
  2. Marks microbial surfaces for destruction by coating them with C3b
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11
Q

How are antibodies a part of innate immune response?

A

Produced by B cells can bind to bacteria but cannot kill bacteria alone

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12
Q

How are soluble proteins a part of innate immune response?

A

in the serum can complement the activity of antibodies or can act alone

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13
Q

How are complement proteins a part of innate immune response?

A
  1. Made primarily by the liver and travel in the blood and lymph
  2. Coat the surface of extracellular bacteria or virus particles
  3. Aid in the phagocytosis of microbes by myeloid phagocytic cells
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14
Q

What do complement components circulate as?

A

Zymogens

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15
Q

What is proteolytic cleavage?

A

The activation of zymogens and complements

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16
Q

What amplifies protease activation?

A

The number of protein molecules activated are increased

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17
Q

What happens when 1 complement component is activated by a previous?

A

The active site becomes exposed

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18
Q

What is the difference between a and b on a complement protein other than C2?

A

a is little piece, floats away and has biologic activity
b is big piece, attached to nearest membrane

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19
Q

What pathways generate complement protein C3b?

A
  1. Alternative
  2. Lectin
  3. Classical
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20
Q

What pathway is antibody dependent?

A

Classical

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21
Q

How is the classical pathway activated?

A
  1. Complexes of IgG or IgM antibody with antigen on the pathogen surface or CRP
  2. 2 IgG must be bound
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22
Q

What is CRP?

A

Soluble protein released from the liver and is an indicator of inflammation

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23
Q

What are IgG and IgM?

A

Classes of antibodies produced by plasma cells in response to antigens

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24
Q

What is the difference between IgM and IgG?

A

IgM: efficient at activating complement due to its structure
IgG: most abundant immunoglobulin in blood (3 week half-life)

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25
Q

Describe how IgM binds to antigen?

A

IgM binds up to 10 antigens on the surface of the pathogen and therefore, only the 1 IgM is needed to activate classical pathway

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26
Q

Describe the initiation of classical pathway by antibody binding?

A
  1. C1q initiates a cascade of reactions enabling the next reaction in the sequence
  2. C1 binding is followed by cleavage of C4, then C2
  3. C4b2a bound to the cell surface is C3 convertase
  4. C3 convertase cleaves many C3 proteins that deposit on the surface of the pathogen
  5. Some combine with C3 convertase to form C5 convertase (C4b2a3b)
  6. C5 convertase cleaves C5 protein
  7. This initiates the terminal pathway
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27
Q

What pathway is antibody independent?

A

Lectin and alternative

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28
Q

How is Lectin pathway mediated?

A

Plasma mannose-binding lectin complex (MBL)

29
Q

What are lectins?

A

Proteins tha bind foreign (non-self) carbs that serve as docking sites of mannose binding lectin associated serine proteases (MASPs)

30
Q

What makes lectin different from classical?

A

MASP binds directly to polysaccharides/glycoproteins on the pathogen instead of binding to antibody-antigen complex

31
Q

Where are lectins the most prevalent?

A
  1. Bacterial surfaces
  2. Yeast
  3. Parasites
  4. Some viral particles
32
Q

Describe the lectin pathway?

A
  1. When MASP binds to bacterial surface it can cleave C4 and C2 to form C3 convertase.
  2. This then activates the remainder of the classical pathway.
  3. MASP-4-2-3
33
Q

What makes alternative pathway different from the other two?

A
  1. Spontaneously activated without binding to antibodies to microbial cell wall structures on the surface of pathogens
  2. Responds very quickly to pathogen entry into the body
34
Q

Describe the activation of the alternative pathway?

A
  1. C3 is spontaneously hydrolyzed to C3(H2O) and binds to Factor B
  2. C3(H2O) and Factor B complex is cleaved by Factor D to form the short-lived alternative C3 convertase.
  3. Most is hydrolyzed and inactivated but stabilizing proteins are produced to prevent the inactivation of the short lived C3 convertase
  4. Stabilized C3 convertases cleave C3 into C3a and C3b.
  5. C3b covalently binds to the pathogen surface.
  6. C3b will bind to any surface that lacks inhibitors to block its activity
  7. C3b can be rapidly degraded unless it can be stabilized on the pathogen surface.
  8. C3b binds to factor B and then factor D cleaves factor B into Bb and Ba (diffuses away).
  9. C3b joins with Bb to form C3bBb which forms an alternative C3 convertase than hydrolyzes another C3 to C3a and C3b yielding C3b2Bb (C3bBb3b).
  10. C3b2Bb (C3bBb3b) is the alternative C5 convertase that converts C5 to C5a and C5b and initiates the terminal pathway
35
Q

How can the alternative pathway assist lectin and classical?

A

Amplifies pathways by forming an alternative C3 converts (CC2bBb) not formed by the spontaneous hydrolysis of C3

36
Q

What happens when more C3b is formed by the alternative pathway?

A

An amplification loop is formed to increase more rapid C3b production allowing greater deposition of C3b molecules on the pathogen

37
Q

How is alternative C3 Converts stabilized?

A
  1. Alternative C3 convertases (C3bBb and C3(H2O)) are short-lived and subject to inactivation by hydrolysis.
  2. Properdin (Factor P) stabilizes C3 convertases when bound to the pathogen surface.
  3. Factor P increases the speed and power of complement activation.
  4. Neutrophils make and store properdin (Factor P) in their granules and release this protein when activated by the presence of pathogens
38
Q

What is the terminal pathway-lytic pathway?

A

When all pathways converge at the generation of C3b used to form the C5 converts complex the cleaves C5 into C5a and C5b

39
Q

What cleaves C5 into C5a and C5b for all three pathways?

A

Classical and Lectin Pathways: C4b2a3b
Alternative Pathway: C3b2Bb

40
Q

What is formed after the terminal pathway?

A

membrane bound C5b

41
Q

What is the purpose for C5?

A

Initiates the generation of the Membrane Attack Complex (MAC)

42
Q

What occurs during the terminal pathway assembly phase?

A
  1. C5b binds to C6 and 7 all of which have amphiphilic regions that allow insertion into the membrane.
  2. C8 binds to C7 then initiates the polymerization of many C9s that form a pore complex in the target cell membrane creating the membrane attack complex (MAC).
43
Q

What is the function of MAC?

A

Disrupts osmotic integrity resulting in cell death by cell lysis

44
Q

What are negative regulatory proteins?

A

protect host (self) cell membranes from inappropriate complement attack

45
Q

What are regulatory proteins?

A

Determine the extent and site of C3b deposition

46
Q

What is the function of Decay Associating Factor (DAF/CD55) and Membrane Cofactor Protein (MCP/CD456)?

A

Found on healthy human cell surfaces and will attract Factor I

47
Q

What is the function of Factor 1?

A

Protease that will dissociate C3bBb (C3 convertase) and forming the inactive iC3b which inhibits the alternative pathway on human cell surfaces

48
Q

What is the function of Factor H?

A

Plasma protein that competes with Factor B by binding to C3b and recruiting Factor I to convert C3b to the inactive iC3b

49
Q

Why is regulatory proteins necessary?

A

So that normal cells are not lysed by complement proteins

50
Q

What is the function of C1 inhibitors?

A

binds to activated C1 preventing C1q activation for classical

51
Q

What is the function of C4-binding proteins?

A

displaces C2a from C4b preventing C3 convertase formation (classical and lectin)

52
Q

What is the function of Protectin/Membrane Inhibitor of Reactive Lysis (CD59)?

A

prevents formation of MAC on human cell surfaces by preventing C8 recruitment of C9s to from pore (all pathways)

53
Q

List the biological functions of complements?

A
  1. Lysis of foreign organisms by MAC complex
  2. Opsonization and Phagocytosis
  3. Activation of Inflammation and Chemotaxis of Leukocytes by Complement Anaphylatoxins
  4. Clearance of Immune Complexes from Circulation
  5. Apoptotic Cell Clearance
54
Q

What occurs during Lysis of foreign organism by MAC complex?

A
  1. Lyses bacterial cells especially gram-negative bacteria
  2. Lyses viruses especially enveloped viruses
  3. Some bacteria have developed ways to get around complement
55
Q

What gives E. coli and Salmonella their effectiveness?

A

Developed smooth phenotypes that have very long LPS chains than act to prevent MAC insertion into their membranes

56
Q

What occurs during Opsonization and Phagocytosis?

A
  1. C3b deposits on the surface of microorganism
  2. Macrophages and neutrophils have complement receptors (CR1) bind to their ligand C3b and facilitate phagocytosis of the C3b coated pathogen
57
Q

What is opsonin?

A

Antibody or protein that binds to microbes marking them for phagocytosis

58
Q

What is opsonization?

A

Phagocytosis and elimination of pathogens that are tagged by opsonins

59
Q

What complement proteins are involved with the activation of Inflammation and Chemotaxis of Leukocytes by Complement Anaphylatoxins?

A

(C3a, C4a, C5a)

60
Q

What do anaphylatoxins mediate?

A
  1. Smooth muscle contraction
  2. Increased vascular permeability
  3. Histamine and other inflammatory mediator release from mast cells
61
Q

What is the function of C3a in activation of Inflammation and Chemotaxis of Leukocytes by Complement Anaphylatoxins?

A

C3a can also attract these innate immune cells but is less potent than C5a.

62
Q

What occurs during activation of Inflammation and Chemotaxis of Leukocytes by Complement Anaphylatoxins?

A
  1. C3a or C5a can cause granulocytes to migrate to the area of infection
  2. Cause release of granular contents as well as production of reactive oxygen species in order to destroy the pathogen
63
Q

What occurs during Clearance of Immune Complexes from Circulation?

A
  1. Immune complexes form when antibodies bind to soluble antigens.
  2. C3b bind to the Fc region of the immune complex
  3. C3b (bound to the immune complex) is recognized by the CR1 receptor on RBCs which transports the immune complexes to the spleen and liver where they are phagocytized by resident macrophages
  4. RBCs are then returned to circulation.
  5. Complement and RBC work together as a transport system
64
Q

What occurs during Apoptotic Cell Clearance?

A
  1. Mannose-binding lectin and C1q can bind debris of apoptotic (dying) cells
  2. Cellular debris is removed through binding of these complement proteins to the C1qR and CR1 receptors on phagocytic cells.
  3. Complement is acting as a transport to clear dying cells.
65
Q

The complement cascade can be divided into what 2 phases?

A

Activation and formation of C3b
Formation of MAC complex

66
Q

What is the purpose of MAC complex formation?

A

creates a pore in the pathogen membrane leading to lysis

67
Q

What are the complement proteins of the MAC complex formation?

A

C5b, C6-9

68
Q

What disruptions can trigger inflammation and cell lysis?

A
  1. Inappropriate initiation
  2. Patient has deficiencies in complement components or regulators
69
Q

What causes excessive complement activity?

A

Associated with inflammatory and autoimmune diseases

Immunology (17 decks)

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