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Block 6 Week 1 > Antigen Recognition by T Cells > Flashcards

Antigen Recognition by T Cells Flashcards

1
Q

What is the reactive lymphocytes in the blood during mononucleosis caused by epstein barr virus?

A

T cells, not B cells

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2
Q

EBV is a persistent and chronic infection of (blank) cells

A

B

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3
Q

The CTLs recognize EBV proteins located (intracellular/extracellularly) of chronically infected B cells

A

intracellularly (in the nucleus)!!!

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4
Q

There are (blank) major types of T cells and their roles

A

6

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5
Q

T cell receptors are (blank-beta) or (gamma-(blank) chain dimers

A

delta

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6
Q

CD (blank) is on all T cells

A

3

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7
Q

T cells are (always resting/active) until antigen stimulated

A

resting until stimulated

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8
Q

When do T cells proliferate?

A

upon antigen stimulation, then able to mediate functions

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9
Q

How long do T cells last?

A

a lifetime

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10
Q

Do memory T cells act quickly when re-stimulated by an antigen?

A

no, they must be restimulated, proliferate, then they can mediate functions

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11
Q

What are the 6 T cell subsets?

A 
4 types of CD4 T helper cells
-TFH
-TH1
-TH2
-TH17
AND
CD4 T regulatory cells
AND
Cytotoxic T cells CD8
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12
Q

What does TFH (follicular helper) do?

A

cells produce growth factors for B and T cells

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13
Q

What does TH1 do?

A

increases cytotoxic T cell activity

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14
Q

What does TH2 do?

A

increases antibody production; switch to IgE

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15
Q

What does TH17 do?

A

brings neutrophils to site

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16
Q

What does CD4 T regulatory cells do?

A

regulate proliferation of normal T and B responses

suppresses autoimmunity

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17
Q

What do cytotoxic T cells CD8 do?

A

kill cells infected with viruses

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18
Q

Where do you find follicular helper T cells?

A

you find these CD4 T cells in lymphoid follicles in spleen, lymph nodes peyers patches (small intestine)

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19
Q

How do follicular helper T cells divide?

A

they must recognize and antigen then they can divide

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20
Q

What is the function of follicular helper T cels?

A

provide cytokines required for T and B cell proliferation and are used for memory

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21
Q

What do follicular helper T cells produce?

A

IL-2 (a growth factor for all T and B cells) IL-4, IL-5, and interferon g

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22
Q

If you lack CD4 T helpers what can you leave your self susceptible to?

A

getting AIDS!!!!!

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23
Q

(blank) cells support T cell division and direct B cell functions

A

TFH CD4 T cells

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24
Q

Why is the loss of CD4 T helper cells critical in the development of AIDS?

A

This decline will result in a decline and loss of IL-2 secretion and thus T/B cell activation and proliferation.

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25
Q

Where do you find TFH in the spleen?

A

in the periarteriolar lymphoid sheath

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26
Q

What does CD4 Th1 secrete?

A

gIFN (mainly) and IL-2

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27
Q

What does CD4 TH2 secrete?

A

IL-4 and IL-5 and IL-2

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28
Q

Where do you find B cells in the spleen?

A

in the germinal center

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29
Q

What is the main function of CD4 Th1 cells?

A

activate infected macrophages, provide help to B cells for antibody production, support CD8 cytotoxic activity

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30
Q

What is the main function of CD4 TH2 cells?

A

provide help to B cells for antibody production, especially switiching to IgE

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31
Q

How can you differentiate between CD4 TH1 and TH2?

A

different cytokine production and TH1s support CD8 cytotoxic activity

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32
Q

TH1 and TH2 can (blank) the immune response.

A

polarize

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33
Q

TH1 and TH2 can polarize the immune response, what does this mean?

A

meaning that depending on which TH cell is activated the immune response can be driven more cellularly (via Th1 response) or more humoral (via the Th2 response).

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34
Q

(blank) is the signature cytokine that distinguishes a TH1 cell from TH2 and TH17 cells

A

Gamma interferon

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35
Q

(blank) is the signature cytokine that distinguishes a TH2 cell from TH1 and TH17 cells.

A

IL-4

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36
Q

(blank) is the signature cytokine of TH17 cells that distringuishes TH17 cells from TH1 and TH2 cells.

A

IL-17

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37
Q

TH1 responses drive (blank) immune responses

A

cellular (main goal is to make cytotoxic granules)

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38
Q

TH2 responses drive (blank) immune responses

A

humoral

i.e main goal is to make antibodies

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39
Q

T or F

many different cell types have receptors for gamma interferon

A

T

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40
Q

Gamma interferon is the (type I/type II) interferon.

A

type II (i.e cannot use alph and beta interferon receptors)

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41
Q

Do B cells have receptors for gamma interferon? What does this mean?

A

yes

cause B cells to slow proliferation and to switch to IgG isotypes

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42
Q

What cell types have receptors for IL-4?

A

B cells and eosinophils

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43
Q

What does interferon gamma do?

A

IFNγ is an important activator of macrophages and inducer of Class II major histocompatibility complex (MHC) molecule expression

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44
Q

(blank) polarize T helper 1 or T helper 2 cell differentiation (and individual biases)

A

cytokines

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45
Q

(blank) from dendritic cells and macrophages direct conversion from TH0 (immature effector T cell) to TH1

A

IL-12

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46
Q

What releases IL-12 to allow from the conversion rom TH0 (immature effector T cell) to TH1

A

dendritic cells and macrophages

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47
Q

(blank) from ACTIVATED mast cells and TH2 cells directs THO conversion into TH2

A

IL-4

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48
Q

What releases IL-4 to direct THO conversion into TH2?

A

activated Mast cells and TH2 cells

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49
Q

(blank) control intracellular mycobacterium tuberculosis that cause TB, which is unaffected by Ab’s

A

TH1 T cells

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50
Q

How does THI T cells control TB?

A

beating it up intracellularly

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51
Q

Mycobacterium tuberculosis prevents formation of (blank)

A

phagolysosomes

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52
Q

How do delayed type hypersensitivity T helper 1 cells kill bacteria?

A

it uses gamma interferon to instruct macrophages to kill bacteria inside the macrophages

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53
Q

What are delayed type hypersensitivity TH1 cells?

A

these are memory TH1 cells that were previously sensitized to the antigen, proliferated and became quiescent memory cells until they re-encountered their cognate antigen

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54
Q

Are delayed type hypersensitivity responses (DTH) quick?

A

no they take about 48 hours

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55
Q

What happens around 18 hours in the DTH response?

A

you get leakage of plasma into the skin site and fibrinogen is activated to fibrin.

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56
Q

In the DTH response when you get leakage of plasma into the skin and this is coupled with fibrin, what happens?

A

You get induration which is when a FIRM lesion forms

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57
Q

When does induration peak?

A

24-48 hrs after antigen introduction

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58
Q

What happens to macrophages when under the influence of TH1?

A

they become multinucleated

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59
Q

Memory TH1 cells take how long after activation to make gamma IFN? When does the macrophage response occur?

A

more than 4 hours

hours after this response

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60
Q

When macrophages are induced to multinucleate by TH1 cells, what else do they do?

A

Make TNF alpha and other inflammatory cytokines and then make the skin response

NOTE::::: Macrophages make the skin response!!!!

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61
Q

What are the 2 essential cell types in DTH?

A

macrophages and TH1 T

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62
Q

What are memory CD8 T cells?

A

they are cells that when activated again will release granulysin which kills intracellular bacteria.

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63
Q

What does granulysin (the cytotoxin released from CD8) need to enter infected cells so they an kill stuff?

A

perforin

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64
Q

What are some examples of DTH immunopatholoy type IV responses?

A

poison ivy and nickel allergies (these are memory responses)

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65
Q

Control of TB bacteria; elimination of other bacteria is done by what?

A

CD4 TH1 and DTH

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66
Q

Long term control of TB and clearance of intracellular bacteria is done by what?

A

CD8 and CTL (w/ perforin and granulysin)

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67
Q

(blank) mediate delayed type hypersensitivity (DTH), our defense against bacteria that live inside macrophages.

A

TH1 cells

68
Q

What are some intracellular bacteria that TH1 cells can kill with DTH?

A

mycobacterium TB, M. leprae, listeria, salmonella, erlichia

69
Q

T or F

infected macrophages themselves can kill their bacteria

A

T

70
Q

How can infected macrophages themselves kill their bacteria?

A

they must be activated by antigen specific CD4+ memory TH1 cells

71
Q

Why wont you see DTH on first exposure to a TB vaccine?

A

because you need a prior exposure to get your TH1 numbers up high enough to create DTH memory T cells

72
Q

What is the antigen in the TB skin test?

A

PPD (purified protein derivative)

73
Q

How do you get the DTH response in the TB skin test?

A

memory DTH TH1 CD4 cells recognize PPD and you get a macrophage inflammatory response which causes skin inflammation

74
Q

What is the delay for DTH in skin tests? why?

A

about 48 hrs

it takes time for 2 cell types to activate: resting memory Th1 cells and macrophages

75
Q

In DTH, resting memory Th1 cells must induce what?

A

mRNA and make gamma IFN

76
Q

In DTH, what do the macrophages make?

A

mRNA, iNOS and TNFalpha

77
Q

What do T helper 2 T cells secrete and what does this allow for?

A

IL4, drives B cell to produce IgE

78
Q

(blank) and (blank) are critical in control of helminths

A

IL-3 and IL-9

79
Q

What does IgE do?

A

it arms mast cells and can mediate ADCC (antibody dependent cellular cytotoxicity)

80
Q

TH2 cells drive mast cell recruitment against helminths via (blank) and (blank)

A

IL3 and IL9

81
Q

IgE arms mast cells against (blank)

A

helminths

82
Q

Mast cells produce mediators such as ….?

A

histamine, TNF alpha, MMCP (these recruit inflammatory cells and remodel the mucosa)

83
Q

(blank) cell follicles are also found in tonsils and appendix

A

B

84
Q

What do Thelper17 Ts secrete?

A

IL-17

85
Q

What is the key activity of Th17?

A

to activate fibroblasts, epithelial cells and keratinocytes to produce inflammation and bring in neutrophils

86
Q

The cells with receptors for IL-17 are inducible to secrete many (blank) cytokines

A

inflammatory

87
Q

The nuclear transcription factor RORγt is the master regulator of (blank).

A

TH17 differentiation

88
Q

How do you get Th17 to secrete IL 17 and then what happens once it gets secreted?

A

a dendritic cell must secrete TGF beta which will tell IL17 to make fibroblasts secrete CXCL8 which will make neutrophils kill bacteria?

89
Q

CD 4 T regulatory cells are antigen-specifc in (blank) but often antigen-nonspeific in their (blank).

A

elicitation

effects

90
Q

T or F
In other words, it takes a specific antigen to induce a Treg (T regulatory cell) to secrete suppressive factors. It does not secrete suppressive factors constitutively.

A

T

91
Q

What would happen without T regulation?

A

overactive immune system, large lymph nodes and enlarged spleen

92
Q

Identify 7 types of lymphocytes that divide in response to specific antigens

A

TFH, THI, TH2, TH17, CD8, CTL, CD5 regulatory T cell, B cell

93
Q

Excess T regs in fulminant TB will produce (blank)

A

clinical anergy

94
Q

How do you turn off gamma IFN production?

A

IL-10 from Tregs

95
Q

What does TGF beta do?

A

turns of all proliferative responses

96
Q 
What does this:
Patients are unable to respond to:
tuberculin skin test
Candida skin test
new antigens, e.g., the dye DNCB,
     (dinitrochlorobenzene) as a reactive  chemical that will elicit DTH responses
A

TGF beta and IL-10 when there is an excess of T regs

97
Q

What leads to the inability to produce any new memory or memory response?

A

too much T regulatory cells

98
Q

(blank) is a term in immunobiology that describes a lack of reaction by the body’s defense mechanisms to foreign substances, and consists of a direct induction of peripheral lymphocyte tolerance.

A

anergy

99
Q

What does this:

ehances neutrophil response, promotes barrier integrity (skin, intestine)

A

CD4 Th17 cells

100
Q

What suppress T cell responses?

A

CD4 regulatory T cells

101
Q

What does CD4 regulatory T cells secrete?

A

IL-10 and TGF beta

102
Q

Where do you find perforin?

A

in killer lymphocytes and NK cells

103
Q

How do you get a CTL cell to kill?

A

needs to bind a MHC 1 peptide and an antigen and must proliferate to be effective

104
Q

What besides being killing machines can CTLs do?

A

thye can generate (resting) memory cells

105
Q

What cytokines do CTLs need to be effective?

A

IL-2l IL-15 an IL-21

106
Q

CTL killing is dependent on what?

A

cytotoxic granules w/ perforin
OR
membrane molecules of the TNF receptor family (FasL, TRAIL)

107
Q

When CTLs kill, do they die with the cell they destroy or can they keep killing?

A

They can keep killing

108
Q

How can CTLs destroy viral mRNA within an infected cell without killing the cell?

A

by using gamma interferon

109
Q

If a CTL decides to kill an infected cell how does it do it, by apoptosis or necrosis?

A

it can do it either way

110
Q

If a CTL decides to kill an infected cell via necrosis, how does it do it?

A

it damages the outside of the cell and irreversibly damages the plasm membrane

111
Q

If a CTL decides to kill an infected cell via apoptosis, how does it do it?

A

damages the cells insides and keeps the plasma membrane intact

112
Q

(blank) is the disruption of the PM of a cell and can occur at the beginning or end of the death process. (blan) leaks out of the cell

A

lysis

cytoplasm

113
Q

(blank) is a form of cell death in which the cell is injured by external events. The cell itself is passive and just dies of injury.

A

necrosis

114
Q

(blank) is a form of cell death in which a cell is induced to commit suicide and dies from the inside out. The plasma membranes are often left intact: the dead cell fragments into membrane-enclosed pieces which are cleared by phagocytic macrophages and neutrophils. This form of death has advantages since intracellular contents (for example, viruses) remain contained within membranes. Prior to the cell death, the nucleus appears condensed, the cell shrinks, and the plasma membrane blebs.

A

apotosis

115
Q

Is it dangerous to be near a CTL when it is doing its killings?

A

no, innocent bystanders are fine and the killing is rapid.

116
Q

How do CTLs make a cell undergo apoptosis?

A

they can polarize their cytotoxic granules toward the infected cell and the cell kills itself
OR
Can bind FasL to Fas on the infected cell which ill induce a cascade that starts apoptosis

117
Q

(blank) and (blank) are released from the CTL granules. These are also released by (blank) cells in innate immunity and ADCC function

A

perforin
granyzme
NK

118
Q

How do CTLs recognize only infected “targets”?

A

Dual recognition via a specific TCR to MHC 1 and viral peptides

119
Q

To memory CTLs have FasL and cytotoxic granules?

A

no, they need IL-2 or other cytokines to induce these molecules

120
Q

What is in the cytotoxic granules of CTLs?

A

perforin, granzyme A, granzym B, granulysin

perforin creates the pore in the membrane to put the enzymes in

121
Q

Perforin can fuck up a cells life 2 ways. what are they?

A

cause membrane disruption that causes immediate necrosis
OR
makes a pore so cytotoxic enzymes can enter

122
Q

Granule-mediated death can cause apoptosis when (blank) or (blank) enter into the target cell via perforin permeability

A

granzymes A

granzymes B

123
Q

Once granzyme A or B enter a cell, how do they make the cell undergo apoptosis?

A

they cleave procaspases (by Grz B) or caspase-activated DNAse inhibitor (by Grz A)

124
Q

Most CD8 T cells kill what?

A

viruses

125
Q

Most CD8 T cells are anti-viral but (blank), faciliated by perforin, from CD8 CTLs can also kill TB bacteria

A

granulysin

126
Q

The CD8 cytotoxic T cells respond with perforin an granulysin for long term defense to (blank)

A

TB

127
Q

Can dead vaccines stimulate CTL? WHy is this important?

A

no only live vaccines

because you need live vaccines to be able to create viral imunity so you can make CTL memory cells

128
Q

What will dead vaccines give you?

A

antibodies but no CTLs. This is no good for viral infections because antibodies cannot control viral replication once the virus is inside the cell.

129
Q

Patients w/ diGeorge syndrome can fight off (blank) infections but not (blank) infections, why?

A

bacterial
viral
because DiGeorge affects your T cell production

130
Q

DiGeorge Syndrome is a congenital malformation caused by defective development of the (blank) and (blank) pharyngeal pouches.

A

3rd and 4th

131
Q

What organs does diGeorge syndrome effect?

A

thymus, parathyroid (low calcium, tetany), and heart

has low T cells and has antibodies present

132
Q

How come DiGeorge patients are susceptible to not only viral infections, but to mycobacterial and fungal infections?

A

due to there 22q deletion they do not make enough T cells. Helper T cells activate macrophages to arrest TB and neutrophils to be more effective at killing yeast and fungi. WIthout the T cells you have weak protection

133
Q

How can you cure DiGeorge?

A

graft with a younger than 14 week old fetus. (has to be young so you wont get Mature T cells that will cause graft host disease)

134
Q

What is a conjugate?

A

making something that is not immunogenic into something that is and allows your body to produce an antibody to it (i.e attaching a bacteria to a sugar so that everytime you have that sugar you will elicit an immune response)

135
Q

TCRs have (blank) recognition

A

dual

recognition of peptide and recognition of MHC

136
Q

(blank) and (blank) initiate recognition signals in TCRs when a peptide (Ag) has bound

A

CD3 and CD8

137
Q

Why are recognition signals awesome for researchers to mess with?

A

because it allows you to compromise a T cell receptor by either blocking the signals or not allowing the receptor to get both signals so you can compromise the immune response

138
Q

If a T cell makes an anti-self TCR what happens to it?

A

it is deleted or unresponsive

139
Q

How can you displace a self peptide on an APC?

A

you can overwhelm it with a large amount of a substituted peptide

140
Q

THe MHC class (blank) proteins hold peptides for CD4 T cells

A

II

141
Q

how long are antigen peptides?

A

20-30 AAs long

142
Q

The MHC class II alpha and beta cain dimer forms a binding site for (blank) peptides that “hang out” at the ends of the site.

A

larger

143
Q

T or F

Each MHC II allele can bind thousands of different peptides and interact with thousands of different T cells.

A

T

144
Q

The MHC class (blank) proteins hold peptides for CD8 T Cells

A

I

145
Q

What is the structure of an MHC I protein?

A

single alpha chain w. a beta2 microglobulin

146
Q

THe MHC class I alpha chain forms a (blank) that binds peptides. What size peptides can fit into this?

A

cleft

peptides smaller than 11 AAs

147
Q

Each MHC I allele can bind thousands of different peptides and interact with thousands of different T cells
T or F

A

T

148
Q

The peptides fit into the MHCI cleft by (covalent/non-covalent) “anchoring” of several amino acids of the peptides into the cleft. The N terminal AA of the peptide rarely anchors. Two internal amino acids of the peptide and the C terminal AA anchor. (think of anchors and seas) Since different MHCI alleles have different clefts formed by their different sequences, they anchor differ peptides.

A

non-covalent

149
Q

Does MHC1 or MHC2 hold smaller peptides?

A

class 1

150
Q

What are the 2 co-receptors for antigens that determine binding to MHCII and MHCI ?

A

CD4 and CD8

151
Q

How do CD4 and CD8 intitate signaling?

A

via kinases when the TCR binds tightly to a MHC

152
Q

CD4 cells bind only to MHC (blank) and CD8 cells bind only to (blank)

A

II

I

153
Q

How does a T cell recognize a nonpeptide antigen?

A

CD1s found on APCs can present lipid antigens

154
Q

Which T cells can recognize CD1 molecules (non peptide antigens)

A

CD4 neg and CD8 neg

can detect TB

155
Q

Both CD4 and CD8 cells require co-stimulation (in addition to Ag) for responses. What are the 2 signals. (also they require danger signals IL-1/TNFalpha)

A

Signal 1: antigen

Signal 2: B7 interacting with T CD28

156
Q

What is B7?

A

it is CD80 and CD86 on APCs ad activated B cells

157
Q

When T cells only get one signal what happens?

A

they die or become anergic

158
Q

(blank) is on the APC and (blank) is on the T cell

A

B7

CD28

159
Q

When an APC secretes TNF alpha and IL-1, what does this mean? Why is this important?

A

they are sending out Danger signals

you need these for T cell responses

160
Q

What do T and B cell receptors have in common?

A

2 chains
variable binding sites at end of receptor
receptors have short intra cytoplasmic tails
other molecules perform transembrane signaling

161
Q

Which type of receptor is this, B or T?

Have Ig receptors that recognize native ag structures

A

B

162
Q

Which type of receptor is this, B or T?

Recognize “processed” proteins (peptides)

A

T

163
Q

Which type of receptor is this, B or T?

Receptor is unchanged in AA sequence for the life of that cell

A

T

164
Q

Which type of receptor is this, B or T?

May later secrete proteins similiar to their ag receptor proteins (Ab’s without ig transmembrane domain)

A

B

165
Q

Which type of receptor is this, B or T?

Undergo gene mutation for affinity maturation of the receptor and Ig

A

B

166
Q

T or F

Co-stimulatory receptors and their counter-ligans differ for T and B cells

A

T

167
Q

What are the 2 costimulatory signals for b cells?

A

CD40

activated T cell

Block 6 Week 1 (13 decks)

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