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Block 6 Week 1 Colt > L2&3 Antigen Recognition by T Cells - Hudig > Flashcards

L2&3 Antigen Recognition by T Cells - Hudig Flashcards

1
Q

Macrophages and dendritic cells direct conversion from Th0 to (blank)

A

Th1

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2
Q

ACTIVATED mast cells and Th2 cells direct conversion from Th0 to (blank)

A

Th2

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3
Q

What IL is used in the conversion from Th0 to Th1?

A

IL-12

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4
Q

What IL is used in the conversion from TH0 to Th2?

A

IL-4

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5
Q

What are the five types of CD4 positive t cells?

A
  1. TFH
  2. TH1
  3. Th2
  4. Th17
  5. CD 25 regulatory
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6
Q

What cytokines do TFH cells release?

A

IFNg, IL2, IL4, IL5

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7
Q

Where do you find TFH cells?

A

spleen, lymph nodes, Peyer’s patches, and in the periarteriolar lymphoid sheath of white pulp

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8
Q

What is the function of the cytokines released by TFH?

A

growth factors for B and T cells

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9
Q

What role does TFH play in B cell development?

A

supports isotype switching and Ab production

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10
Q

How many fold can an Ag-specific T cell increase after stimulation?

A

10,000x

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11
Q

What is the function of TH1 cells?

A

increases the cytotoxic activity of CD8 t cells; causes pre-CTLs to mature into CTLs; activates infected macrophages to kill intracellular bacteria

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12
Q

What cytokine does Th1 release?

A

IFNg ONLY

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13
Q

Does TH1 drive cellular or humoral immunity?

A

cellular

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14
Q

How does Th1 activate macrophages?

A

releases IFNg which tells the macrophage to kill the bacteria inside of it

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15
Q

T/F: TB is not affected by Ab production

A

true

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16
Q

What reaction are memory Th1 cells involved in?

A

Delayed type hypersensitivity reaction

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17
Q

What is the function of TH2 cells?

A

Increases Ab production, helps B cells switch to IgE production

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18
Q

what cytokines does Th2 release?

A

IL4 ONLY

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19
Q

IgE from B cells arms (blank) cells and drives ADCC (which stands for blank)

A

mast cells

antigen dependent cell mediated cyototoxicity

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20
Q

What cytokines does TH2 release to control helminths? What cells do they target?

A

IL3 and IL9, target mast cells

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21
Q

What do mast cells release in response to IL3 and 9 from Th2 cells?

A

histamine, TNF-a, and MMCP

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22
Q

What is the big picture goal of the activated mast cells from Th2 cells?

A

Recruit inflammatory cells and remodel the mucosa

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23
Q

Do Th2 cells drive cell mediated or humoral immunity?

A

Humoral

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24
Q

B cells and (blank) cells both have IL4 receptors

A

eosinophils

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25
Q

IL4 receptors on B cells allow them to (blank)

A

proliferate and begin Ab production

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26
Q

What is the function of TH17 cells?

A

brings neutrophils into the site, activates resident fibroblasts, epithelial cells, and keratinoctyes to produce inflammation`

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27
Q

The effectors of TH17 actions are a good example of a cytokine (blank)

A

network

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28
Q

What is the function of IL017?

A

promotes bacterial killing

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29
Q

TGF-beta and IL-6 from (blank) cells stimulates TH17 to divide

A

dendritic cells

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30
Q

When signaled by DC with TGF-b, TH17 releases IL-17 which targets (blank) cells

A

fibroblasts

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31
Q

The fibroblasts targeted by the IL17 of Th17 release (blank and blank) to activate neutrophils

A

CXCL8 and CXCL2

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32
Q

What cells is the end-effector of TH17 action?

A

Neutrophils killing the bacteria sensed originally by the Dc

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33
Q

What is the master regulator of TH17 differentiation?

A

RORyt

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34
Q

What other CD protein are Tregs positive for?

A

CD25

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35
Q

Tregs have a high affinity for the (blank) receptor?

A

IL2

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36
Q

T/F: Upon leaving the thymus, Tregs are the only cells that are CD25 postive

A

true

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37
Q

T/F: after Ag encounter, other T cells become CD25 positive

A

True

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38
Q

Why do other cells become CD25 positive after Ag encounter?

A

to increase affinity for the IL2 receptor to increase ability to proliferate

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39
Q

What is the function of Tregs?

A

Regulate proliferation of normal T and B cell responses

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40
Q

T/F: Tregs are capable of suppressing autoimmunity

A

true; important in SLE

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41
Q

What are the only cells that secrete suppressive factors?

A

Tregs

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42
Q

(blank) suppresses activated APCs from making cytokines

A

IL10

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43
Q

(blank) suppresses lymphocyte proliferation

A

TGF-b

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44
Q

Treg activation leads to less (blank and blank) rlease from Th cells, resulting in less lymphocyte proliferation and CTL granule release

A

IFNg and IL2

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45
Q

What is the critical transcription factor for Tregs?

A

Foxp3

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46
Q

Treg activation is antigen (specific/nonspecific), but its actions are antigen (specific/nonspecific)

A

specific, nonspecific

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47
Q

What cell type can produce clinical anergy, as seen in a negative skin TB test while having positive sputum?

A

Tregs

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48
Q

Explain how Tregs cause clinical anergy?

A

IL10 turns off IFNg production, TGF-b turns off all proliferation, Pts can’t respond to skin test or new Ag stimulation to DTH

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49
Q

What cell type kills cells infected with viruses?

A

CTL CD8

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50
Q

What MHC class does CD8 use?

A

MHC I

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51
Q

What do all cells (except RBCs) use for MHC?

A

MHC II

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52
Q

What three cytokines do CD8 cells need to become cytotoxic?

A

IL2, IL5 (both from TFH?), and IL-21

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53
Q

what two cytokines stimulate CD8 proliferation and granule production?

A

IL2 and IFNg

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54
Q

What proteins are in the TNF receptor family on CD8 cells?

A

FasL and TRAIL

55
Q

What MHC II chain components bind the peptide? What CD type uses this?

A

the a1/b1 chains; used by CD4

56
Q

How long is the Ag peptide for MHCII?

57
Q

Describe the alpha/beta dimer of the MHCII?

58
Q

MHCII binds (intra/extra) cellular peptides?

A

extracellular

59
Q

On MHC I, what chain components bind the peptide?

60
Q

Describe the MHC I configuration?

A

a1a2a3/b2-microglobulin

61
Q

What is the size of the protein bound in the MHC I cleft?

A

11 aa or smaller

62
Q

T/F: peptides bind to MHC covalently

A

FALSE; noncovalently

63
Q

Describe the way the peptide binds to the MHC?

A

binds at the peptide C terminus and anchors using a few amino acids

64
Q

MHC I binds (intra/extra) cellular components

A

intracellular

65
Q

The CD protein binds to the (blank) while the TCR binds to the (blank)

A

CD to MHC, TCR to Ag

66
Q

Binding of both the peptide and the MHC is known as dual recognition and stimulates (blank) signaling

67
Q

For T cells, what is signal 1?

68
Q

For T cells, what is signal 2?

A

co-stimulatory signal
B7-1 aka CD80 (signal; APC)
B7-2 aka CD86 (signal; APC)
to CD28 (receptor; t cell)

69
Q

What do you need besides signals 1 and 2 to get T cell activation?

A

IL-1/TNF-a innate danger signal

70
Q

Do B cells use the same signal 2 as T cells?

71
Q

What is the similarity between Ig molecules and TCR structurally?

A

both have 2 CHAINZ, both bind the Ag/Ab at the end of the receptor chain, both have short intracytoplasmic tails, both use 2nd messenger cascades

72
Q

Do B cells recognize native or processed structures?

73
Q

Do T cells recognize native or processed structures?

74
Q

The (TCR/Ig) undergoes affinity mutation

75
Q

Compare an AB to the Ig molecule?

A

Ab is an Ig molecule missing the transmembrane domain

76
Q

What is the signal 2 for B-cells?

A

CD40L (signal; t-cell) to CD40 (receptorl; B cell)

77
Q

What macromolecule does CD1 present to T cells?

A

bacterial lipids; important for TB!

78
Q

What is the only cell type that expresses CD1?

79
Q

What is the CD profile of a T cell responding to CD1 activated APC?

A

CD4/CD8 negative!

80
Q

What type of chain does the TCR of the CD1 responding T cell have?

A

alpha/beta

81
Q

All people have the same (CD1/MHC proteins) and huge variation among (CD1/MHC proteins)

A

same CD1, lots of MHC variation

82
Q

What immunologic concept does diGeorge syndrome illustrate?

A

as it affects T-cells, it shows that you need more than just Abs to control infection

83
Q

What types of infections are diG pt’s susceptible to?

A

Viral, mycobacterial, an fungal

84
Q

What types of infections can diG pt’s fight?

85
Q

T/F: diG pts will produce Abs

86
Q

What is a PREVENTABLE cause of diG?

87
Q

Compare T cell levels in diG and SCID?

A

diG: low
SCID: low

88
Q

Compare B cell levels in DiG and SCID?

A

diG: normal
SCID: low

89
Q

Compare serum Ig levels in diG and SCID?

A

diG: normal
SCID: low

90
Q

What is the cause shitty T cells in diG?

A

missing branchial pouch 3 and 4, therefore no thymus!

91
Q

What is the cause of shitty T-cells in SCID?

A

No IL-7 production and potentially bad RAG genes; mutation in the common gamma chain of the cytokine receptors

92
Q

What cell is the end-effector of the activity of Tfh?

93
Q

What cell is the end-effector of the activity of Th1?

A

macrophages and B cells

94
Q

What cell is the end-effector of the activity of Th2?

A

eosinophils and B cells

95
Q

What cell is the end-effector of the activity of TH17?

A

epithelial cells and neutrophils

96
Q

What type of pathogen stimulates TFH?

97
Q

What type of pathogen stimulates TH1?

98
Q

What type of pathogen stimulates TH2?

A

helminthic parasites

99
Q

What type of pathogen stimulates TH17?

A

immunologic reactions

100
Q

(blank) cell type is important in MS, IBS, RA, and other autoimmune disorders

101
Q

What cell type mediates the DTH response?

102
Q

DTH is specific to what four pathogens?

A
  1. mycobacterium tuberculosis
  2. M. leprae
  3. Listeria
  4. Salmonella
  5. Erlichia
103
Q

Is the DTH response active upon first-time Ag exposure?

A

No, the TH1 must have been previously sensitized to the Ag, proliferated, then went dormant

104
Q

What is the function of the Th1 cell in DTH?

A

Immediate control of the TB and elimination of other bacteria

105
Q

How does Th1 control TB in DTH?

A

production of IFNg which stimulates infected macrophages to kill the bacteria within themselves

106
Q

How long does it take for Th1 to begin to produce IFNg during the DTH? Why?

A

4 hour minimum; they were dormant and need to up gene regulation

107
Q

Upon IFNg stimulation in DTH, describe what the macrophage does to control its TB infection?

A

Secretes TNF-a

Converts iNOS to NOx and creates ROS (microbicidal), but some TB persists and becomes latent

108
Q

The cytokines from which cell actually causes the response in DTH?

A

The macrophages!! The Th1 just induces the macrophages to release their cytokines

109
Q

What is the minimum time required for a DTH response? What is happening during this time?

A

18 hours; dormant Th1 wakes up, makes mRNA for IFNg, then more time for the macrophages to make mRNA for iNOS and express TNF-a

110
Q

What are the clinical findings of the DTH?

A

leakage of plasma into skin, activation of fibrinogen to fibrin

111
Q

What is the name of the firm lesion in DTH?

A

induration

112
Q

At what time does DTH peak?

A

24-48 hours post Ag introduction

113
Q

How doe the macrophages change morphologically during the DTH?

A

they become multinucleate

114
Q

What are two common items that cause DTH?

A

poison ivy and nickel allergies

115
Q

In alternate macrophage stimulation, what does TH1 do?

A

stimulates microbicidal activity

116
Q

In alternate macrophage stimulation, what does TH2 do?

A

stimulates macrophages to begin tissue repair and ECM protein synthesis

117
Q

What three cytokines inhibit microbicidal activity and suppress TH1 immunity?

A

IL4, IL10, and IL13

118
Q

How do CTLs cure a cell without killing it?

A

they release IFNg which instructs the cell to destroy the viral mRNA

119
Q

Is apoptosis or necrosis favorable for viral infections? Why?

A

Apoptosis; virions are always membrane-bound

120
Q

Perforin and granzymes are also released from (blank) cells in innate immunity and in ADCC function

121
Q

Which cell has FasL and which has Fas?

A

Target cell has Fas, CTL has the FasL (I AM THE KEYMASTER, ARE YOU THE GATEKEEPER?)

122
Q

Does the Fas system trigger apoptosis or necrosis?

123
Q

Do resting CD8 cells have the FasL or granules?

124
Q

What stimulates CD8 cells to produce FasL and granules?

A

IL-2 (and maybe IFNg?) to produce them

125
Q

What are the contents of the cytotoxic granules?

A

Perforin
Granzymes A/B
Granulysin

126
Q

What does perforin do?

A

Creates a channel to let in the granzymes and causes an osmotic defect in the PM allowing Ca and H into the cell

127
Q

Which granule content is able to kill TB bacteria?

A

granulysin

128
Q

What two granule contents are necessary for long term TB control?

A

perforin and granulysin

129
Q

Which granzyme cleaves procaspase?

130
Q

Which granzyme cleaves the inhibitor of caspase activated DNase?

131
Q

granule mediated cell death causes necrosis when (blank) lyse the cell membrane

A

polyperforins

132
Q

What is the only type of vaccine that will boost memory CTLs?

A

LIVE vaccines

133
Q

T/F: live vaccines are highly effective

Block 6 Week 1 Colt (11 decks)

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