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old "mic 661" > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

What is the central cell in the primary immune response?

A

DC

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2
Q

What is the central cell in the secondary immune response?

A

T/B cells

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3
Q

What 3 things is special about the secondary immune response?

A

diversity
specificity
memory

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4
Q

What are the 4 steps of the primary immune response?

A
  1. antigen—DC interactions
  2. DC—T cell interactions
  3. antigen—B cell interactions
  4. T cell—B cell interactions
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5
Q

What are the 3 functions of DCs?

A
  1. pathogen recognition via PRR
  2. phagocytosis using PRR
  3. antigen processing
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6
Q

Which MHC presents intracellular pathogens?

A

MHC I

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7
Q

Which MHC presents extracellular pathogens?

A

MHC II

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8
Q

Where are MHC I peptides loaded?

A

ER

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9
Q

Where are MHC II peptides loaded?

A

vesicles

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10
Q

What MHC does CD8+ T cells recognize?

A

MHC I

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11
Q

What MHC does C4+ T cells recognize?

A

MHC II

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12
Q

What cells express MHC I?

A

all cells

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13
Q

What cells express MHC II?

A

macrophages
DC
B cells
TEC

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14
Q

What does the symmetry of MHC I look like?

A

asymmetrical

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15
Q

What does the symmetry of MHC II look like?

A

symmetrical

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16
Q

Does MHC I or II bind smaller peptides?

A

MHC I

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17
Q

Where does mature DC go after interacting with pathogen?

A

SLT

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18
Q

What does DC present antigens on?

A

MHC II

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19
Q

What cell does DC present to?

A

T cells

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20
Q

What co-stimulatory molecule do DCs upregualte when presenting to T cells?

A

B7

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21
Q

Where is the location of antigen presentation & B/T cell interactions?

A

SLT

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22
Q

How do T cells come across a DC presenting an antigen?

A

They flow through the blood and SLT and will stay in the SLT if it comes across the DC presenting it will stay and differentiate and proliferate

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23
Q

What 3 ligand/receptor interactions happen when a T cell interacts with a DC?

A
  1. TCR—MHC
  2. CD4 or CD8 —-MHC
  3. CD28—B7
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24
Q

What autocrine cytokine signaling induces T cell proliferation?

A

IL-2

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25
Q

What 3 things can T cell differentiate into?

A

cytotoxic T cells
T regs
T helper

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26
Q

What allows isotype switching and SHM in BCR?

A

RNA splicing of heavy chain

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27
Q

memory and naive B cells express membrane bound ______

A

IgG

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28
Q

Naive B cells specifically express membrane bound _____ and _____

A

IgM
IgD

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29
Q

Where does class switching occur on BCR?

A

Fc regions heavy chain

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30
Q

B cells present to T cells which is required for…

A

T cell dependent B cell activation

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31
Q

What are the 3 ligand/receptor interactions that occur when B and T cells interact?

A
  1. TCR—MHC
  2. CD4—MHC
  3. CD40-L—CD40
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32
Q

T cells upregulate _______ that interact with CD-40 on B cells

A

CD40-L

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33
Q

What is it called when a T cell and B cell are interacting?

A

conjugate pair

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34
Q

Where do B cells undergo SHM and isotype switching in the body?

A

germinal centers

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35
Q

What do memory B cells express?

A

membrane bound BCR

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36
Q

Do memory B cell receptors undergo class switching and SHM?

A

a little but not much

37
Q

Do plasma cells BCR under class switching and SHM?

A

yes

38
Q

What type of B cells are inactivated during the secondary immune response and why?

A

naive B cells
they are very broad and we already have a specific antibody from primary exposure

39
Q

What are the 3 isotypes involved in Type II HSR?

A

IgG1
IgG3
IgM

40
Q

What does IgG1 and IgG3 do?

A

opsonize
activate NK cells
activate complement

41
Q

What does IgM do?

A

activate complement

42
Q

What are the 3 effector function of type II HSR?

A

apoptosis
lysis
phagocytosis

43
Q

What is the definition of a type II HSR?

A

IgM/IgG recognizes innocuous cell surface molecules as foreign, leading to antibody-mediated cell death via 3 mechanisms

44
Q

What are the 3 mechanisms that cause cell death in type II HSR?

A
  1. Ab-mediated complement activation = MAC
  2. ADCC via NK cells
  3. Ab-mediated opsonization = phagocytosis
45
Q

What Ig isotype is responsible for the Ab-mediated complement activation mechanism in type II HSR?

A

IgM

46
Q

What part of IgM binds to pathogen surface for complement activation?

A

Fab

47
Q

What part of IgM recognizes C1q in complement activation?

A

Fc region

48
Q

What is activated that leads to MAC formation?

A

C5 convertase

49
Q

What conformational change occurs to IgM for complement activation?

A

pentameric IgM curls “staples”

50
Q

What are the steps of complement activation?

A
  1. C1q binds to antigen bound IgM
  2. IgM conformational change = activation of C1r and Crs
  3. C3 convertase hydrolyzes C3
  4. C5 convertase formed
  5. C1s cleaves C4 & C2 & C4b binds C2 exposing C1s
  6. C1s cleaves C2 = c4b2a
  7. C3b (in C5 convertase) binds to C5 = C4b2a cleaving C5 into C5a and C5b
  8. C5b starts MAC complex
51
Q

What is the key molecule in complement that starts the MAC complex?

A

C5b

52
Q

What Ig isotype is mainly used in ADCC?

A

IgG1

53
Q

What region of Ab bind to pathogen’s surface?

A

Fab

54
Q

What receptor do NK cells express during ADCC that binds to Ab Fc region?

A

FcGRII

55
Q

What 2 things do NK cells release in ADCC?

A

granzymes and perforin

56
Q

What is the steps of Fas-L/Granzyme mechanism?

A
  1. Fas-L activates caspace-8
  2. granzyme B & caspace-8 cleaves Bid
  3. Bid mediates the release of cytochrome c
  4. granzyme-b is cleaved = activation caspace-3
  5. apoptosis
57
Q

How do Ab function as an opson?

A

coats pathogen surface to be phagocytosed

58
Q

Phagocytes have ___ receptors so it can bind to Ab when its acting as a opsin

A

Fc receptors

59
Q

What are 2 phagocytes?

A

macrophages
neutrophils

60
Q

What digests pathogens in phagocytes?

A

lysosomes

61
Q

What are 3 types of type II HSR?

A
  1. mismatch blood transfusions
  2. hemolytic disease in newborns
  3. drug induced anemia
62
Q

What happens during a mismatch blood transfusions?

A

IgM binds to blood antigens (b/c its wrong) causing RBC lysis

63
Q

What happens during hemolytic disease in newborns?

A

IgG responds to D-allele of Rh antigen

64
Q

What happens during drug induced anemia?

A

IgM binds to RBC = RBC lysis

65
Q

What Ig isotype is used in mismatched blood transfusions and drug induced anemia?

A

IgM

66
Q

What 2 Type II HSR have the same mechanism?

A

mismatched blood transfusions
drug induced anemia

67
Q

What enzymes do RBC express?

A

glycosyltransferase

68
Q

What expressed on RBC makes the persons blood type?

A

glycoproteins

69
Q

What individuals wont have hemolytic type II reactions and why?

A

type O
they lack A&B antigens

70
Q

What is the only small difference between blood types?

A

additions of one sugar

71
Q

Most people express Ig___ Ab againsy blood carb antigens they don’t express

A

IgM

72
Q

Why do do people possess IgM against blood types they dont have?

A

common microbes express similar carb antigens that induce host B cell responses = Ab binding to A or B antigen that isn’t thier own

73
Q

What Ig isotype mediates complement mediated lysis of RBC?

A

IgM

74
Q

What is dangerous about RBC lysis?

A

high levels of hemoglobin that breaks down into porphyrin which metabolizes to toxic billirubin

75
Q

Why is the fetus being Rh+ (D-allele) not an issue before the child is born?

A

there are little Rh+ RBC that are passed from bay to mother so no immune response happens

76
Q

When does having an Rh+ baby and Rh- mother become and issue and why?

A

at birth when blood mixes
Rh+ baby blood induces an IgM immune response in the Rh- mother to clear the Rh+ fetal blood

77
Q

How does the mother’s immune system create protection for re-exposure of Rh+?

A

the mother will generate anti-D memory B cells which generate IgG for next exposure

78
Q

Why is a mother’s secondary exposure of D+ easier to achieve with fewer D+ RBC than the first exposure?

A

she has memory B cells which have a lower threshold for activation

79
Q

In the secondary exposure of D+ RBC it takes _____ D+ RBC to activate an immune response

A

fewer

80
Q

Ig___ cannot pass between placental barrier

A

IgM

81
Q

Ig___ can pass the placental barrier

A

IgG

82
Q

In hemolytic disease in fetus, Ig___ is responsible for the primary response while Ig___ is for the secondary response

A

IgM
IgG

83
Q

Why is it dangerous that IgG can cross the placental barrier?

A

IgG is responsible for the secondary response (MEMORY) and is able to cross the barrier
- very dangerous for 2nd pregnancy

84
Q

What does it mean the fetal RBC are attacked?

A

mothers anti-D antibodies bind to fetal Rh+ RBC and fetus own NK cells lyse fetal RBC

85
Q

Rhogam is given during _______ pregnancy to prevent mother’s Ab for binding to fetal RBCs

A

first

86
Q

Why is Rhogam given to mothers 24-28 weeks in pregnancy?

A

almost complete maturation of fetal immune system

87
Q

How does Rhogam therapy work?

A

contains anti-RH (D antigen) Ab that bind to fetal Rh+ RBC and inactivate fetal Rh before they stimulate an immune response in mother

88
Q

What 2 ways does Rhogam prevent primary immune response to Rh+ RBC?

A
  1. inhibit B cell signaling via FCGRIIB
  2. Anti-D Ab binds to fetal RBC and is phagocytosed

old "mic 661" (19 decks)

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