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OLD "MIC 661" > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

How long does the primary response take to clear a pathogen?

A

14 days

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2
Q

What cell type is prominent in the primary response?

A

DC

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3
Q

How long does it take the secondary response to clear a pathogen?

A

3 days

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4
Q

What cell type is prominent in the secondary response?

A

T/B cells

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5
Q

What 3 things are special about the secondary response?

A

diversity
memory
specificity

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6
Q

What are the 4 steps of the primary response?

A
  1. antigen—–DC interaction
  2. DC —— T cell interaction
  3. antigen —— B cell interaction
  4. T cell —— B cell interaction
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7
Q

What are the 3 functions of DCs?

A
  1. pathogen recognition
  2. phagocytosis
  3. antigen processing
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8
Q

How do DCs recognize pathogens?

A

PRR

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9
Q

What MHC presents intracellular antigens?

A

MHC I

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10
Q

What MHC presents extracellular antigens?

A

MHC II

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11
Q

What MHC presents smaller peptides?

A

MHC I

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12
Q

What cell recognizes peptides presented on MHC I?

A

CD8+ T cells

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13
Q

What cell recognizes peptides presented on MHC II?

A

CD4+ T cells

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14
Q

What cells present MHC I?

A

all cells

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15
Q

What cells present MHC II?

A

antigen presenting cells
(DC, B cells, macrophages, TECs)

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16
Q

What does MHC I look like?

A

asymmetrical (2 alpha subunits as peptide binding groove)

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17
Q

What does MHC II look like?

A

symmetrical (alpha and beta subunit as peptide binding groove)

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18
Q

What are the steps of DC presenting antigen to T cells?

A
  1. immature DC encounters pathogen
  2. DC travels to SLT and phagocytoses pathogen
  3. B7 is unregulated on DC
  4. DC presents peptide to T cell on MHC II
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19
Q

What is the place for antigen presentation and B/T cell activation?

A

SLT

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20
Q

How does a T cell find a presenting DC?

A

T cells cycle through the blood and into the SLT and if it doesn’t find a presenting DC in SLT it will re-enter bloodstream

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21
Q

What 3 molecular interactions occur when DCs present to naive T cells?

A

TCR—–MHC
CD4 or CD8
CD28—-B7

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22
Q

What cytokine induces T cell proliferation via autocrine signaling?

A

IL-2

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23
Q

What causes SHM and class switching in BCR?

A

RNA splicing of heavy chain

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24
Q

Memory B cells and naive B cells express _______ Ig

A

membrane bound Ig

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25
Q

Naive B cells express membrane bound Ig___ and Ig___

A

IgM
IgD

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26
Q

Where does class switching occur on BCR?

A

Fc heavy chain

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27
Q

Where does SHM occur on BCR?

A

Fab heavy chain

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28
Q

When B and T cells interact, who presents to who?

A

B cell presents antigen (from DC) to T cell

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29
Q

Why is B and T cell interactions important?

A

required for T cell dependent B cell activation

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30
Q

What 3 molecular interactions occur when B and T cells interact?

A

B cell —— T cell
1. MHC II —–TCR
2. MHC II —– CD4
3. CD40 —– CD40L

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31
Q

What is up regulated on B cells when its MHC interacts with TCR?

A

CD40

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32
Q

What are the steps of germinal center formation?

A
  1. DC presents to naive T cell (in T cell zone)
  2. T cell activated
  3. Naive B cell (in follicle) interacts with follicular DC
  4. B cell processes and presents antigen (MHC II)
  5. T cell interacts with B cells MHC (in cortex) = conjugate pair
  6. T cells differentiate
    Memory B cells (IgM secerted)
  7. OR… B cell reenters follicle and forms germinal center (class switching and SHM)
  8. plasma cells made and secrete different Ig’s
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33
Q

Do memory B cell’s BCR do class switching/SHM?

A

a little but not much

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34
Q

Do long-lived plasma cells do class switching/SHM?

A

yes

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35
Q

What kind of B cells are inactivated in the secondary immune response and why?

A

naive B cells
- not specific

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36
Q

What 3 isotypes are important for T2HSR?

A

IgG1
IgG3
IgM

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37
Q

What do IgG1 and IgG3 do?

A

opsonization
activate NK cells
activate complement

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38
Q

What does IgM do?

A

complement activation

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39
Q

What are the 3 basic functions of T2HSR?

A
  1. apoptosis
  2. lysis
  3. phagocytosis
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40
Q

What is a T2HSR?

A

IgM/IgG recognizes innocuous cell surface molecules as foreign leading to 3 Ab mediated cell death

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41
Q

What are the 3 Ab mediated cell death mechanisms of T2HSR?

A
  1. complement activation (MAC)
  2. ADCC (NK cells)
  3. opsonization (phagocytosis)
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42
Q

What isotype is important for Ab-mediated complement activation?

A

IgM

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43
Q

In Ab-mediated complement activation, what part of IgM binds to pathogen surface?

A

Fab

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44
Q

In Ab-mediated complement activation, complement ______ recognizes Ab Fc region

A

C1q

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45
Q

In Ab-mediated complement activation, C1q binding to Ab Fc region causes activation of…

A

C1s
C1r

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46
Q

In Ab-mediated complement activation, activation of C1r and C1q leads to _________ = MAC = lysis

A

C5 convertase

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47
Q

In Ab-mediated complement activation, when C1q binding site is exposed the IgM pentamer is in the _________ form

A

staple

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48
Q

COMPLEMENT ACTIVATION STEPS
SKIP

A

SKIP FOR NOW

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49
Q

What molecule initiates the MAC formation?

A

C5b

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50
Q

What isotype is used for ADCC?

A

IgG1

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51
Q

How does the receptor involved in ADCC work?

A

FCGRII binds to Fc of IgG1 (whose Fab is bound to cell surface)

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52
Q

What receptor does NK cells express for ADCC?

A

FcGRII

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53
Q

What enzyme is involved in FAS-L / granzymes mechanism?

A

caspace

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54
Q

In Ab-mediated opsonization, what part of Ab binds to cell surface and which part binds with phagocyte?

A

cell surface: Fab
phagocyte: Fc

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55
Q

What are 2 phagocytes?

A

macrophages and neutrophils

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56
Q

In Ab-mediated opsonization, where are the cells degraded?

A

lysosomes

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57
Q

What are the 3 types of T2HSRs?

A
  1. mismatched blood transfusions
  2. hemolytic disease in newborns
  3. drug induced anemia
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58
Q

What isotype does mismatched blood transfusions use?

A

IgM

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59
Q

How does mismatched blood transfusions work?

A

IgM binds to blood antigens and lysis of blood cells

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60
Q

What isotype does hemolytic disease in newborns use?

A

IgG

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61
Q

What is hemolytic disease in newborns?

A

IgG of mother recognizes RH+ RBC of fetus and binds to fetal RBC and fetal NK cells recognize IgG bound and kills RBC

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62
Q

How does drug induced anemia work?

A

IgM binds to RBC causing RBC lysis

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63
Q

What isotype does drug induced anemia use?

A

IgM

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64
Q

What blood type is not affected by hemolytic disease?

A

type O (lack antigens on surface)

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65
Q

What makes blood types special from one another?

A

glycoproteins of RBC surface

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66
Q

What is the backbone antigen on RBC surface?

A

H antigen

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67
Q

Most people possess _______ Ab against blood carb antigens they don’t express

A

IgM

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68
Q

Why do people have IgM Ab against other blood types that aren’t thier own?

A

common microbes express similar carb antigens that induce host immune response

69
Q

Why is RBC lysis dangerous?

A

hemoglobin is released from RBC which metabolizes into toxic billibrubin

70
Q

What are the steps of hemolytic disease in newborns?

A
  1. FIRST PREGNANCY: Rh+ RBC activate mother’s B cells to produce anti-Rh IgM (cannot cross placental barrier)
  2. SECOND PREGNANCY: On secondary exposure, anti-Rh IgG can cross the placental barrier and attach to Rh+ fetal RBC causes lysis via fetal NK cells
71
Q

How does Rho Gam therapy work?

A

Anti-Rh antibodies bind and inactivate fetal Rh antigens to prevent mother’s cell from recognizing them

72
Q

What 2 mechanisms does Rho Gam use to prevent mothers immune system from recognizing RH+ RBC?

A
  1. FcGRIIB receptor will prevent B cell signaling
  2. Anti-D antibodies bind to RH+ RBC causing macrophage to phagocytose RBCs
73
Q

What are DT4 HSRs?

A

Skin permeable antigens activate CD4+/Th1 cells resulting in sensitization followed by DT4 HSR on second exposure

74
Q

What does the “delayed” come from in DT4 HSR?

A

required recruitment and activation of macrophages

75
Q

DT4 HSR are Th__ cell-mediated macrophage activation

A

Th1

76
Q

What cell is important for DT4 HSR?

A

macrophages

77
Q

What are the polarizing cytokines for DT4 HSR?

A

(Th1)
IL-12
IFN-g
IL-18

78
Q

What are the effector cytokines of DT4 HSR?

A

(Th1)
IFN-g
TNF

79
Q

What are the effector mechanisms of DT4 HSR?

A

(Th1)
cell mediated immunity (barrier protection)
macrophage activation
inflammation

80
Q

What are DT4 HSR antigens?

A

intracellular antigens
contact antigens

81
Q

What 3 things happen during the sensitization phase of DT4 HSR? (first exposure)

A
  1. antigen processing and presentation by MHC II
  2. IL-2mediated differentiation of naive Th0 to Th1 cells
  3. development of memory T cells
82
Q

PPD / mycobacterium induces a ……

A

pure Th1 immune response

83
Q

What are the 3 types of memory T cells in DT4 HSR?

A
  1. central MTC
  2. effector MTC
  3. resident MTC
84
Q

Where are central MTC located?

A

circulate blood/SLT

85
Q

What memory T cell is is specific for one antigen?

A

central MTC

86
Q

Where are effector MTC located?

A

circulate blood / SLT / tissue

87
Q

Where are resident MTC located?

A

in tissue (return to site of infection)

88
Q

What does it mean when resident MTC are “bleeding”?

A

not all resident MTC go to site of infection, some go to other tissues in case there is another infection elsewhere

89
Q

What T cell has CD45RA?

A

naive T cells

90
Q

What T cells have CD45RO?

A

all memory T cells

91
Q

What T cells have CCR7?

A

naive T cells
central MTC
(for trafficking to SLT)

92
Q

What T cell has CD103?

A

resident MTC
(expressed on epithelial cells)

93
Q

Where are monocytes located?

A

blood

94
Q

Where are macrophages located?

A

tissue

95
Q

_________ and _________ come from granulocyte-monocyte progenitors

A

monocytes
neutrophils

96
Q

macrophages develop from ___________

A

monocytes

97
Q

Macrophages produces ______ to recruit monocytes from blood which differentiate into macrophages

A

CCL2

98
Q

What happens in the effector phase of DT4 HSR? (second exposure)

A
  1. APC present to memory Th1 cells
  2. memory T cells produce INF-g/TNF
  3. INF-g/TNF = recruitment of monocytes/macrophages
99
Q

What are the initiators of the effector phase of DT4 HSR?

A

Th1 cells

100
Q

What cytokines induce recruitment of macrophages in the effector phase of DT4 HSR?

A

INF-g/TNF

101
Q

What do macrophages present to in the effector phase of DT4 HSR?

A

memory Th1 cells

102
Q

_____ induces MHC expression in macrophages for the effector phase of DT4 HSR?

A

IFN-g

103
Q

What kills a the pathogen in macrophages?

A

RNS/ROS

104
Q

What secretes INF-g/TNF to activate macrophages in effector phase of DT4 HSR?

A

TH1 cells

105
Q

The secretion of IFN-g/TNF in the effector phase of DT4 HSR, causes a inflammatory ______

A

loop

106
Q

Draw out the inflammatory loop in the effector phase of DT4 HSR?

A
  1. IL-12 induces more Th1 cells
  2. TNF-g induces macrophage activation and vascular permeability
  3. IL-8 neutrophils recruitment
  4. CCL2 monocyte recruitment
  5. IL-6 and IL-1 induces inflammation/fever
107
Q

What cytokines are in the inflammatory loop in the effector phase of DT4 HSR?

A

TNF
IL-12
IL-8
IL-6
IL-1
CCL2

108
Q

What does IL-6 and IL-1 induce in the inflammatory loop in the effector phase of DT4 HSR?

A

inflammation and fever

109
Q

What does IL-12 induce in the inflammatory loop in the effector phase of DT4 HSR?

A

recruitment of more TH1

110
Q

What does IL-8 in the inflammatory loop in the effector phase of DT4 HSR?

A

neutrophil recruitment

111
Q

What does chronic macrophage activation due to inability to eliminate pathogen cause?

A

granuloma formation

112
Q

What are granulomas?

A

multi-nucleated giant cell of fused immune cells to wall off pathogen from tissue

113
Q

What are foam cells?

A

macrophages that have ingested large amounts of lipids (in granulomas)

114
Q

What 2 materials can cause granulomas?

A

silica and sutures

115
Q

What happens if a granuloma cannot be cleared?

A

it will rupture and release pathogen causing tissue/blood vessel damage

116
Q

What is the root cause of tissue/blood vessel damage when granulomas rupture?

A

persistent ROS/RNS activation

117
Q

How does TB tests work?

A

PPD is injected into dermis

118
Q

What are TB test reactions mediated by?

A

CD4 / Th1 cells

119
Q

What is the lipid for poison oak?

A

urushiol (covalently binds to proteins)

120
Q

Poison oak can penetrate skin which makes it __________ __________

A

contact dermatitis

121
Q

Poison oak reactions have multiple T cell subsets compared to TB tests but what is it mainly mediated by?

A

CD4 / TH17

122
Q

TB skin tests and poison oak are both types of ….

A

DT4 HSR

123
Q

DT4 HSR are CD___ T cell mediated

A

CD4 T cells

124
Q

CD8 T cells require stronger activation of _____ due to its cytosolic activity

A

B7

125
Q

What 2 ways can DC cells activate CD8 T cells since they need a lot more B7?

A
  1. sequential activation
  2. cross presentation
126
Q

What is sequential activation of CD8 T cells?

A

DC —CD4 T cell interaction increases B7 levels, then DC interacts/activates CD8 T cell

127
Q

What is cross presentation of CD8 T cells?

A

DC—-CD4 T cell interactions, then changes their antigen processing to present on MHC I which can activate CD8 T cells
(present extracellular antigen on MHC I)

128
Q

What is it called in cross presentation when DC switches thier antigen processing to present on MHC I?

A

cytosolic diversion

129
Q

CD4 T cell engagement help CD8 T cells activate by providing paracrine _____ in cross presentation

A

IL-2

130
Q

TCRs recognize just the peptide presented?

A

No, interact with the MHC as well

131
Q

NKT cells recognize ____ presented by ____ on APCs

A

glycolipids
CD1d

132
Q

NKT cells DO NOT recognize…

A

MHC—peptide complex

133
Q

What is different about NKT cell’s TCRs?

A

no memory or diversity

134
Q

How do NKT cells kill?

A

same as NK cells

135
Q

o

A

o

136
Q

How does CD1a present lipids differently than how MHC presents peptides?

A

lipid is buried in CD1d and the A’ roof is what is recognized

137
Q

Is CD1a activated on LC cells when the A’ roof is blocked or unblocked?

A

unblocked

138
Q

What causes A’ roof to be blocked in CD1a?

A

healthy skin lipid head causes steric hinderance

139
Q

What is the term for the A’ roof being blocked and unblocked on CD1a?

A

interference model

140
Q

In the interference model of CD1a, binding of TCR is soley based on _____ not _____

A

CD1a not ligand

141
Q

CD1__ is highly expressed on LC DCs

A

CD1a

142
Q

CD1__ is expressed on NKT cells

A

CD1d

143
Q

What are LC DCs?

A

Specialized DCs in epidermis

144
Q

What are fillagrin linkages?

A

links keratinocytes to build skin layers

145
Q

What linkage in skin is abnormal in atopic dermatitis?

A

fillagrin linkages

146
Q

What does the corneum/corneocytes provide?

A

waterproof surface of skin

147
Q

What are corneocytes?

A

keratinocytes without nucleus

148
Q

Where are regular LC DCs located?

A

epidermis

149
Q

When LC DCs sample a foreign lipid with its CD1a what T cell subset is produced?

A

TH17

150
Q

What are 2 different methods does the skin use to sense urushiol?

A
  1. LC DCs sense urushiol lipids
  2. Dermal DCs sense peptide–urushiol complex
151
Q

The method of LC DCs sensing urushiol lipids uses CD___ / TH___ activation

A

CD4/TH17

152
Q

The method of dermal DCs sensing peptide-urushiol complex MAINLY uses CD___/TH___ activation

A

CD4/TH1
(can use CD8/CTL)

153
Q

How does the skin sense PPD from TB skin test?

A

injected directly into dermis by passing LC DCs and being sensed by dermal DCs and macrophages

154
Q

What are the 2 most common DT4 HSRs?

A
  1. contact dermatitis (poison oak)
  2. TB skin test (mycobacterium)
155
Q

What 4 things are different about the DT4 HSR of a TB test v. urushoil?

A
  1. antigen
  2. antigen recognition
  3. antigen processing
  4. antigen presentation
156
Q

What kind of pregnancy is required for hemolytic disease in babies?

A

Rho - mother
Rho + fetus

157
Q

Why is the first pregnancy not an issue in hemolytic disease but its an issue in the second?

A

IgM cannot cross the placental barrier in the 1st but IgG memory Ab are made which can cross the barrier during the 2nd

158
Q

What does the follow do in the inflammatory loop in the effector phase of DT4 HSRs?
1. IL-12
2. TNF-g
3. IL-8
4, CCL7
5. IL-6/IL-1

A
  1. IL-12: recruits more memory T cells
  2. TNF-g: recruits macrophages & increase vascular perm
  3. IL-8: neutrophil recruitment
    4, CCL7: recruits monocytes
  4. IL-6/IL-1: inflammatory/fever response
159
Q

What isotype is best for activating complement?

A

IgM

160
Q

NKT cells use CD1__ and LC DCs use CD1__

A

NKT: CD1d
LC DC: CD1a

161
Q

Only CD1___ has an A’ roof

A

CD1a (LC DCs)

162
Q

Why is there no diversity for TCR recognizing CD1a—lipids?

A

The A’ roof is the same for all receptors

163
Q

What 2 things are special about NKT cells?

A
  1. Invariant TCR (no diversity)
  2. Only identified glycolipids
164
Q

INF and TNF are important for what 2 things?

A
  1. Macrophage recruitment
  2. Granuloma formation
165
Q

Since dermal DCs dont have CD1a what do they use?

A

PRR

166
Q

What are the 2 possible fates of B cells once a conjugate pair is formed?

A
  1. Becomes memory B cell (secertes IgM)
  2. Becomes plasma cells (isotype switches by returning to germinal center)
167
Q

Th1/CD4 responses involve recruitment of what cell type?

A

macrophages (DT4HSR)

168
Q

Does the TB skin test elicit an immune response from LC DCs or dermal DCs?

A

Dermal DCs (injected into dermis directly)

OLD "MIC 661" (19 decks)

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