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MicroImmuno > Effector Mechanisms of Immunity > Flashcards

Effector Mechanisms of Immunity Flashcards

1
Q

What are the 4 effector functions of antibodies?

A
  1. Neutralization of microbe & toxin
  2. Opsonization and phagocytosis of microbes
  3. Antibody-dependent cellular cytotoxicity (ADCC)
  4. Complement activation
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2
Q

How does neutralization by antibodies occur?

A

Ab binds to the microbe/toxin before it can bind to the cell receptor.

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3
Q

Which antibody is responsible for opsonization of microbes?

A

IgG

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4
Q

What happens after opsonization occurs?

A

Binding of opsonized microbes to phagocyte Fc receptor (FcyRI) activates phagocyte –> Phagocytosis and killing of ingested Ag.

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5
Q

What 2 antibodies are important in Ab-dependent cellular cytoxicity? What does each Ab react against?

A

IgG and IgE

IgG: Coats virally infected cell to be killed by Natural Killer cells
IgE: Binds to Helminth (worm), which draws eosinophils/basophils/mast cells w/ granules

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6
Q

What 2 Ab’s can activate the classical pathway of the complement cascade?

A

IgM & IgG

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7
Q

What happens after IgM and IgG bind with the antigens?

A

They form a complex, which recruits C1.

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8
Q

How is C3 cleaved and what is it cleaved into?

A

C3 is then cleaved by C3 convertase into C3a and C3b.

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9
Q

Describe the characteristics of C3a and C3b.

A

C3a = smaller, diffuses and attracts neutrophils to cascade thru chemotraction

C3b = larger, covalently binds to site of Ab and then pathogen

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10
Q

What activates C5 protease? What happens after the protease is activated?

A

C3b; formation of the Membrane Attack Complex (MAC) and opsonization of the cell or recognition of bound C3b by phagocyte C3B receptor leading to phagocytosis.

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11
Q

How does the Membrane Attack Complex (MAC) react with cells?

A

It punches holes through the cells membrane, creating osmotic shock and lyses of the cell.

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12
Q

What are anaphylatoxins? What complements act this way?

A

They induce mast cell and basophil mediator release, which can cause anaphylactic shock; C5a, C3a, C4a

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13
Q

What are 2 ways to regulate complement (C’) activation?

A
  1. Host cells express membrane anchored C’ regulatory proteins (C3b) that inactivate C’ when it deposits on a host cell.
  2. Plasma contains soluble C’ regulatory proteins that limit the extent of C1 activation.
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14
Q

What is immune complex glomerulonephritis?

A

Damage caused by Ab-Ag complexes deposited in glomerular basement membrane activating C’ –> Recruiting + activating neutrophils

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15
Q

Hereditary angioedema causes deficiency in what? Leading to?

A

Deficiency of C1-INH; causing severe attacks of edema because cascade is more easily activated and more C3a, C5a are made

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16
Q

What happens in complement deficiency of C3?

A

Increase risk of infection by bacteria.

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17
Q

What happens in complement deficiency of C5, C6, C7, or C8?

A

Increase risk of Neisseria infections.

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18
Q

How is IgA transported through epithelium?

A

In the lamina propria it is bounded to poly-Ig receptor where it goes through “transtosis” into lumen of gut/mucosal surface.

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19
Q

How many Ag binding sites are there for IgA in this process?

A

4; 2 IgA per Ig receptor

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20
Q

What antibody gives neonatal immunity and what does the Ab cross to get to the fetus?

A

IgG, crosses placenta and milk across the gut epithelium.

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21
Q

What receptor involves these 2 mechanisms: neonatal immunity and crossing of antibodies to the fetus?

A

Fc receptor FcRn

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22
Q

What type of immunity is conferred in the newborn?

A

Passive immunity

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23
Q

How do antibodies directly affect microbes?

A

They are able to bind to and neutralize microbes and toxins.

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24
Q

How are antibodies able to bind and neutralize microbes + toxins?

A

The antibody binds to the pathogen preventing it from binding to and infecting/killing the host cell.

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25
Q

By what mechanism do antibodies attach to phagocytes during opsonization?

A

The Fc region of the antibodies attaches to Fc receptors on the surface of phagocytes and/or NK cells, specifically FcγRI.

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26
Q

What type of antibody opsonizes microbes?

A

IgG, typically.

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27
Q

What does the antibody signal the phagocyte to do?

A

Ingest and kill the opsonized microbe.

28
Q

Describe antibody-dependent cellular cytotoxicity (ADCC) of an antibody-coated cell.

A

An infected cell exhibiting surface antigens is coated with IgG, it attaches to NK cells via low-affinity FcγRIII, and the infected cell is killed by the NK cell.

29
Q

Describe antibody-dependent cellular cytotoxicity (ADCC) of a helminth.

A

IgE coats the helminth (worm), which attaches to mast cells, basophils, or eosinophils (all of which have FcεRI). Granules that agitate the infecting worm are released, killing the helminth.

30
Q

Which cells have FcεRI?

A

Mast cells, basophils, and eosinophils

31
Q

What are the three pathways by which the complement cascade is activated?

A
  1. Classical pathway
  2. Alternative pathway
  3. Lectin pathway
32
Q

What is a lectin?

A

A protein that can bind to a sugar.

33
Q

Where is complement produced?

A

In the liver.

34
Q

What two complement compounds when activated become “C3 convertase”?

A

C4bC2b and C3bBb

35
Q

What is the function of C3 convertase?

A

To split C3 into C3b + C3a

36
Q

What are the basics of compliment cascade activation that all three pathways share?

A

First, various complement components are activated to generate C3 convertase, which splits C3 into C3a and C3b. C3b activates C5 convertase splitting C5 into: C5a and C5b. C5b causes the formation of the MAC (membrane attack complex).

37
Q

Describe the Classical pathway of complement cascade activation.

A

An IgM or IgG antibody binds to the antigen and this complex along with C1 activates the C4bC2b form of C3 convertase.

38
Q

Describe the Alternative pathway of complement cascade activation.

A

C3b binds to microbial surface and Bb joins to form C3 convertase.

39
Q

Describe the Lectin pathway of complement cascade activation.

A

Mannose binds lectin stimulating the C4bC2b form of C3 convertase.

40
Q

Where is mannose typically found?

A

On yeast.

41
Q

Which complement component is the most abundant?

A

C3

42
Q

Which complement component is larger C3a or C3b? What is the function of each?

A

C3b is larger and functions to activate the complement cascade up to C9, opsonizing the things that it coats. C3a is smaller and diffuses away, acting as a chemoattractant.

43
Q

Describe the presence of complement components in the body.

A

All of the C’ components pre-exist in the blood, with C3 being the most abundant.

44
Q

Which of the Classical and Alternative pathways is more efficient? Why have the less efficient pathway still?

A

The Classical pathway is more efficient. The alternative pathway, while less efficient, does not require the production of antibodies before activation of the complement cascade can begin, thus begins more quickly.

45
Q

What happens to C5a, C3a, and C4a?

A

They diffuse away acting as chemoattractants and cause inflammation by stimulating mast cells + basophils to release their inflammatory mediators.

46
Q

What other complement components join C5b to form the MAC?

A

C6, C7, C8, and many C9s

47
Q

How does the MAC cause cell death?

A

It punches holes in the cell membrane and the cell dies via osmotic lysis.

48
Q

How can the binding of C3b to a microbe cause it to die before activation of the complement cascade?

A

The binding of C3b to a microbe opsonizes it, marking it for phagocytosis.

49
Q

What are C3a, C3a, and C4a known as?

A

Anaphylatoxins

50
Q

How is complement activation regulated? (2 ways.)

A
  1. Host cells express membrane anchored C’ regulatory proteins that inactivate complement when it deposits on a host cell. (Blocks formation of C3 convertase & opsonization).
  2. Plasma contains soluble C’ regulatory proteins that limit the extent of C’ activation.
51
Q

Describe two diseases involving complement overactivity.

A

Immune Complex Glomerulonephritis – damage caused by Ag-Ab complexes deposited in glomerular basement membrane activating C’ and recruiting and activating neutrophils.

Hereditary angioedema - deficiency of C1-INH; causes severe attacks of edema because the cascade is more easily activated and a lot of C3a and C5a are made.

52
Q

Describe known effects of complement deficiencies.

A

A deficiency of C3 causes increased risk of infection by many types of bacteria. Deficiency of C5, C6, C7, or C8 is associated with increased risk of Neisseria infections.

53
Q

Discuss the transport of IgA antibodies through epithelium.

A

A plasma cell produces and secretes IgA, which forms dimeric IgA outside the cell. A poly-Ig receptor on a mucosal epithelial cell binds the dimeric IgA and endocytoses it. The dimeric IgA attached to the receptor is released on the other side of the epithelium via proteolytic cleavage.

54
Q

Where does transport of IgA antibodies through the epithelium occur?

A

On gut or other mucosal surfaces (i.e. the oral cavity)

55
Q

Which antibodies are able to be transported from mother to child?

A

IgG antibodies

56
Q

Where does the transport of antibodies from mother to child happen?

A

Across the placenta to the fetus and from milk across the gut epithelium of the infant.

57
Q

What do both the mechanisms: transport of antibodies from mother to child involve?

A

The neonatal Fc receptor (?)

58
Q

What does transport of antibodies do for the newborn?

A

It confers passive immunity to the newborn.

59
Q

What type of T-cell activates macrophages that contain bacteria to kill the bacteria?

A

Th1 CD4+ T-cells

60
Q

What do they secrete to activate the macrophages?

A

Interferon-γ

61
Q

What are the responses of activated macrophages?

A

Killing of phagocytosed microbes.
Increased expression of MHC molecules.
Costimulators (B7 molecules)
Secretion of cytokines (TNF, IL-1, chemokines, IL-12)

62
Q

What does CTL stand for?

A

CD8+ Effector T-cells

63
Q

What does recognition of MHC class I complexes lead to the release of?

A

Intracellular granules that contain perforin and granzymes

64
Q

What is the function of perforin?

A

It oligomerizes and inserts itself into membrane creating holes.

65
Q

What is the function of granzymes?

A

They are proteases that enter the cell via perforin holes and induce apoptotic cell death.

MicroImmuno (13 decks)

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