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MI and Genomics > MI 04b: Antibody Effector Functions > Flashcards

MI 04b: Antibody Effector Functions Flashcards

1
Q

Ab crossreact with (identical/non-idential) epitopes, with (identical/non-identical) strengh.

A

Non-identical; non-identical

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2
Q

Binding between epitope and Ab depends on which constant(s)?

A

Ka (association) and Kd (dissociation)

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3
Q

Which Ig isotype is the main one in blood?

A

IgG

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4
Q

Which Ig isotype is the main one in mucosa/secretions, such as (X)?

A

IgA;

X = tears, saliva, GI, vaginal, milk, mucus

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5
Q

The most protective Ab are those that bind (X) and cause (Y).

A 
X = part of toxin attachment protein that binds to host cell;
Y = neutralization
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6
Q

Which Ig classes are most important for neutralization?

A

IgG and IgA

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7
Q

(IgA/IgG/IgE) act as (X) by binding/coating microbe and cross-linking (Y) receptors on (Z) cells to activate phagocytosis.

A

IgG;
X = opsonins
Y = Fc(gamma)
Z = macrophages/neutrophils

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8
Q

ADCC (antibody-dependent cell cytotoxicity) involves which Ig class? This is done by cross-linking (X) receptors on (Y) cells.

A

IgG;
X = Fc(gamma) (CD16)
Y = NK cells

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9
Q

List the receptors on NK cell that serve as markers to identify/isolate these cells.

A
  1. Fc(gamma) aka CD16

2. CD56

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10
Q

Why can’t worms be phagocytosed?

A

Too large

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11
Q

(X) Ab and (Y) cell have evolved mainly to confer protection agains worms.

A 
X = IgE
Y = eosinophils
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12
Q

Worm infection induce (X) cells to secrete (Y).

A 
X = Th2 (helper)
Y = IL-4 and IL-5 (cytokines)
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13
Q

In worm infection, the key cytokines produced have which functions?

A 
IL-4: B cells undergo class switch to IgE
IL-5: proliferation/activation of eosinophils
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14
Q

Worm infections involve which Ig class? The Ab coats worm and engages (X) receptors on (Y) cells. This causes (Z).

A

IgE;
X = Fc(epsilon)
Y = eosinophils
Z = exocytosis of eosinophil granules

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15
Q

To increase sensitization of the cells, free (X) Ab can bind to (Y) receptors on mast cells and (Z) cells in which respective locations?

A 
X = IgE
Y = Fc(epsilon)
Z = basophils

Mast cells in submucosa/skin
Basophils in blood

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16
Q

(X) Ab on mast cell encounters antigen, leading to (Y).

A 
X = IgE
Y = exocytosis of granules
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17
Q

Mast cell granules contain mediators of (X). Secretion of these granules (increases/decreases) vascular permeability to allow:

A

X = inflammation;
Increases

Exit of Ab, complement, leukocytes from vascular system to extravascular (infected) space

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18
Q

Mast cell granules contain mediators of (X). Secretion of these granules leads to (increase/decrease) in mucus secretion. Why?

A

X = inflammation;
Increase;
Trap microbes

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19
Q

Mast cell granules contain mediators of (X). Secretion of these granules leads to (increase/decrease) in muscle contraction. Why?

A

X = inflammation;
Increase;
Expels microbes from GI, genitourinary, or respiratory tracts

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20
Q

List the key functions of complement system.

A
  1. Kill/opsonize microbes
  2. Clear immune complexes
  3. Initiate inflammation
  4. Recruit monocytes and neutrophils to infected tissue
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21
Q

List the three pathways of complement system. They primarily differ in (X).

A
  1. Classical
  2. Lectin
  3. Alternative

X = the way they’re activated

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22
Q

(X) complement pathway is activated spontaneously on (host/microbial) surfaces.

A

X = Alternative

Microbial (host cells protected)

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23
Q

(X) complement pathway activated when its first component, (Y), binds terminal (Z) residues on (microbe/host) cell.

A 
X = Lectin
Y = MBL (mannose binding lectin)
Z = mannose

Microbe

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24
Q

(X) complement pathway activated when its first component, (Y), binds (Z) sites on (FAB/Fc) regions of (IgA/IgM/IgG/IgE) Ab.

A 
X = Classical
Y = C1
Z = C1-binding

Fc; IgM and IgG

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25
Q

The complement pathways (converge/diverge) at (X) complement component. They proceed to form/generate deadly (Y) on (host/microbe) membrane.

A

Converge;
X = C3
Y = MAC (membrane attack complexes)

Microbe

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26
Q

MAC consists of which complement components?

A

C5b-C9

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27
Q

Convertase enzymes in complement system function to cleave (X) into (Y). What’s the fate of the products?

A 
X = complement components
Y = a-fragment (diffuses away) and b-fragment (covalently binds to microbe surface)
28
Q

Which key (X) enzymes are required for MAC formation?

A

X = convertase

C3 and C5 convertase

29
Q

C5 convertase is generated by interaction of (X) with (Y).

A 
X = C3 convertase
Y = some C3b molecules
30
Q

Assembly of MAC: (X) complement components join (Y), which is already bound, due to (Y) interaction with (Z).

A 
X = C6-9
Y = C5b
Z = C5 convertase
31
Q

The first components of (X) complement pathways are structurally similar in that they (contain/associate with) (Y).

A 
X = classical and lectin
Y = serine proteases

Classical (C1) contains serine proteases
Lectin (MBL) associates with serine proteases

32
Q

(X) number of IgM molecules sufficient to activate (Y) complement pathway. What about IgG? Why?

A 
X = 1 (has 5 Fcs)
Y = Classical

High density of IgG needed to ensure close proximity of 2 IgG Fcs

33
Q

Activated C1 and MBL/MASP complex have common action of (X). What’s the fate of the products?

A

X = cleave C2 and C4 (into a and b components)

The b components remain bound, and C2b interacts with C4b to form C3 convertase

34
Q

C3 convertase is comprised of:

A

C4b2b (Classical or lectin pathways) or C3bBb (alternative pathway)

35
Q

Spontaneous activation of (X) complement pathway occurs by (Y). This is followed by (Z).

A 
X = alternative
Y = slow, spontaneous hydrolysis of C3 (into a and b components)
Z = binding of Factor B to C3b
36
Q

Alternative complement pathway: following hydrolysis of C3, (X) binds to (Y). Then (Z) comes along and…

A 
X = Factor B
Y = C3b
Z = Factor D

Factor D cleaves Factor B, generating C3bBb (C3 convertase enzyme)

37
Q

MAC formation involves sequential association of (X) with bound (Y). Finally, polymerization of (Z) has which effect in (host/microbial) membrane?

A 
X = C6-8
Y = C5b
Z = C9

Forms hole in microbial membrane (lysis)

38
Q

Which microbe is especially susceptible to complement lysis?

A

Gram negative bacteria

39
Q

The (X) fragment of the complement system is known to covalently attach to (Y) and then bind to (Z) receptors on which specific cells? This allows it to participate in elimination of microbes.

A 
X = C3b
Y = microbe
Z = C3b receptor (aka C1)

Erythrocytes, B cells, phagocytes

40
Q

(X) fragment of complement system, covalently bound to microbe, binds to (Y) receptor on phagocyte. What will the phagocyte do?

A 
X = C3b
Y = CR1
  1. Phagocytose and degrade microbe
  2. Peptide-MHC II display (activating Th cells)
41
Q

(X) complement fragments initiate/amplify inflammation by binding (Y) receptors on (Z).

A 
X = Y = C5a and C3a
Z = mast cells and basophils
42
Q

(X) complement fragments initiates chemotaxis of (Y) to site of infection. Which gradient does (Y) follow?

A 
X = C5a
Y = neutrophils

C5a gradient

43
Q

Decay accelerating factor (DAF) is a(n) (X) that acts by (Y). It’s expressed on most (Z) cells.

A 
X = membrane regulator of complement system
Y = binding C3 convertase (accelerates its dissociation)
Z = blood
44
Q

Factor I is a(n) (X) that acts by (Y). What’s left behind?

A 
X = soluble regulator of complement system
Y = cleaving C3b into small fragments

C3d (ligand of CR2 B cell co-receptor)

45
Q

Spontaneous activation of C1 proteases can be regulated/inhibited by (membrane/soluble) regulator (X).

A

Soluble;

X = C1 inhibitor

46
Q

DAF deficiency leads to complement-mediated (X) of (Y) cells. Name clinical symptoms of this and explain the causes.

A 
X = lysis
Y = erythrocytes
  1. Anemia (low RBC)
  2. Red-colored urine (Hb released from lysed cells and excreted in urine); Paroxysmal nocturnal hemoglobinuria
47
Q

Hereditary angioedema is also known as:

A

C1 inhibitor deficiency

48
Q

Cross-linking of insoluble particles by Ab is called:

A

Agglutination

49
Q

Cross-linking of soluble particles by Ab is called:

A

Immuno-precipitation

50
Q

Ab binds/connects two different antigen molecules.

A

Cross-linking

51
Q

Ab binds similar, but non-identical epitopes.

A

Cross-react

52
Q

Deficiency in (X) complement component predisposes individual to immune complex disease.

A

X = C2, C3, C4

53
Q

Deficiency in (X) complement component predisposes individual to infections from pus-inducing microbes.

A

X = C3

54
Q

Deficiency in C5-C9 complement components predisposes individual to which type of infection?

A

Gram-negative bacteria (Neisseria)

55
Q

Which cell/complement/Ig mediates innate phagocytosis?

A

Neutrophils, macrophages/monocytes

56
Q

Which cell/complement/Ig mediates innate opsonization/immune-complex clearance?

A

C3b

57
Q

Which cell/complement/Ig mediates adaptive opsonization/immune-complex clearance?

A

IgG

58
Q

(Cell-mediated/humoral) immunity is main form of protection against extracellular bacteria/toxins.

A

Humoral

59
Q

(Cell-mediated/humoral) immunity is main form of protection against intracellular bacteria/toxins.

A

Mainly CM (but humoral also important)

60
Q

(Cell-mediated/humoral) immunity is main form of protection against protozoa.

A

Mainly CM

61
Q

(Cell-mediated/humoral) immunity is main form of protection against worms.

A

Humoral

62
Q

(Cell-mediated/humoral) immunity is main form of protection against viruses during early infection.

A

Humoral

63
Q

(Cell-mediated/humoral) immunity is main form of protection against virus, following invasion of host.

A

CM

64
Q

List two viruses that undergo antigenic variation.

A

HIV (***) and Influenza

65
Q

List two bacteria that undergo antigenic variation.

A
  1. Neisseria

2. E. coli

MI and Genomics (16 decks)

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