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immunology > 11. Activation of T lymphocytes > Flashcards

11. Activation of T lymphocytes Flashcards

1
Q

what type of cells are constantly in the blood

A

naive T cells

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2
Q

what are the type of cells that can activate T cells

A

dendritic cells

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3
Q

where do naive T cells go from blood

A

2ndary lymph nodes where they meet dendritic cells

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4
Q

what is the movement from lymph nodes to organ they are needed

A

homing

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5
Q

how do activated T cells get to correct area

A

randomly go through circulation until it get to correct area

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6
Q

what helps to complete T cell differentiation

A

macrophages

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7
Q

what can effector T cells activate

A

Follicular B cells

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8
Q

how do Ag get to lymph nodes

A

mature/ activated Dendritic cells ingest and cleave Ag for presentation on membrane and take from periphery to lymph nodes

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9
Q

how do T cells find correct Ag

A

interact with many until find correct one

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10
Q

where do activated T cells go

A

remain in lymph nodes to help B lymphocytes or migrate to sites of infection to activate macrophages

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11
Q

what is induced by T cell recognizing Ag

A

IL2 secretion and clonal expansion

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12
Q

who do effector CD4+ T cells respond to Ags

A

produce cytokines

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13
Q

what do cytokines from activated CD4+ cells induce

A

recruitment and activation of leukocytes as well as activation of B cells

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14
Q

what is the function of CD8+ cell

A

kill infected or altered cells

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15
Q

what is activated by effector CD 4+ cells

A

macrophages, B cells and inflammation

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16
Q

what are the types of CD 4+ cells

A

effector and memory

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17
Q

CD 8 cells other name

A

cytotoxic T lymphocytes

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18
Q

what types of cells do naive CD 8 cells become

A

effector and memory CD8 cells

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19
Q

how does immune response work against intracellular pathogens

A

kill the host cell with macrophage ingestion then phagocytosis

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20
Q

how long does it take memory cells to differentiate

A

3-5 days so window opportunity due to innate immunity first

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21
Q

fever with no sickness is caused by

A

memory cells

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22
Q

what is induced when T cells have Ag recognition and co-stimulation

A

secrete cytokines, proliferation, differentiation into effector and memory cells

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23
Q

function of effector T cells

A

eliminate microbes and cause tissue damage

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24
Q

what happens after Ag is eliminated

A

T cell response declines

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25
Q

which T cells are long lived cells

A

memory

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26
Q

what is the advantage of memory T cells

A

enhanced ability to react against Ags

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27
Q

three signals for T cell activation

A

Ag recognition, costimulation, cytokines

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28
Q

naive T cells can only be activated by ___________ while effector can be activated by ________________

A

naive by DCs w/ antigen while Effector can recognize Ags presented by tissue macrophages and B cells

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29
Q

TCR activation by APC requires binding of which adhesion molecules

A

LFA1 to ICAM 1, CD2 to CD 48 or 59

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30
Q

inhibitory signal for TCR to APC

A

CTLA 4 to CD 80/86

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31
Q

what is CTLA 4

A

homology of CD 28

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32
Q

activation co-stimulation for signal 2

A

CD 28 to CD 80/86

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33
Q

what is LCK associated

A

CD 4 and 8

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34
Q

what dose LCK do once TCR is active

A

phosphorylates CD 3 and ZAP 70 after it binds P-CD3

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35
Q

what does ZAP 70 do

A

phosphorylates LAT and SLP76

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36
Q

what is the role of LAT

A

recruit GADS and GRB2

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37
Q

what is the role of GRB2

A

phosphorylates and activates PLCy

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38
Q

what does activated PLCy produce

A

IP3 and DAG

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39
Q

what does IP3 activate

A

NFAT and increased Ca2+ via calmodulin/ calneurin pathway

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40
Q

what does DAG lead to

A

activation of PKC to activate NFkB

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41
Q

besides Grab 2 and GADS, what does LAT activate

A

RAS and MAP K for AP!

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42
Q

what does LCK phosphorylate

A

ITAMS of CD3 complex

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43
Q

had do phosphorylated ITAMs cause

A

bring in ZAP 70 by SH2 domains to the P

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44
Q

what happens when ZAP 70 binds ITAM

A

Lck phosphorylates ZAP 70

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45
Q

what does phosphorylation of ZAP 70 cause

A

catalytic activity

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46
Q

what does ZAP-70 phosphorylate

A

LAT and SLP-76

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47
Q

what is the role of SLP 76

A

scaffolds to recruit other signaling molecules

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48
Q

what type of PTK is ZAP70

A

SYK

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49
Q

what do super antigens bind

A

MHC II molecules and V region of B TCR. Only specific TCRs

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50
Q

what is a saying for superantigens

A

glue T cells to APC and activate them

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51
Q

what is the problem of super antigens

A

activate many for massive amounts of cytokines for shock. KEEP T cells bound to MHC and don’t allow release

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52
Q

what can superantigens not do

A

be processed into peptides

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53
Q

example of bacterial superantigens

A

staphylococcal enterotoxins

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54
Q

what to staphylococcal enterotoxins cause

A

food poisoning and Toxic shock syndrome

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55
Q

what is the classification of super antigens

A

mitogens

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56
Q

concentration needed for SAg to cause fever, shock and death

A

less than 0.1 pg/ml

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57
Q

what makes SAg -T cell binding so bad

A

leads to proliferation of more SAg-T cells

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58
Q

what are the pro inflammtory cytokines that cause such problems with super antigens

A

TNF, IL 1 and IL2 for fever and shock

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59
Q

what type of immune response is T cell activation

A

innate immunity

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60
Q

what determines which helper T cells are activated

A

cytokines such as IL2

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61
Q

what activates APCs to produce costimulators

A

microbes and cytokines for innate immunity

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62
Q

what is an example of a costimulator besides CD 28/ CD 80/86

A

B7

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63
Q

which cytokines is signal 3

A

IL 12

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64
Q

what does IL 12 do

A

differentiation of naive T cells into effector cells

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65
Q

what are the anti-apoptotic molecules

A

Bcl Xl and BCL2

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66
Q

what is B7 another name for

A

CD 80

67
Q

what is B7-2 another name for

A

CD 86

68
Q

what is important for T cell costimulation

A

regulation of B7 and CD 80 co stimulators

69
Q

how does CD 28 signals work

A

in cooperation with Ag recognition

70
Q

are CD28 and B 7 the only co stimulators

A

no, many homologs exist and can be positive or negative selection

71
Q

what influences the outcome of T cell activation

A

balance between activation and inhibitory receptors of CD 28 family

72
Q

what is the goal of T cell activation

A

handle infection without causing tissue damage

73
Q

what part of TCR activation do APCs express

A

ligands such as B7-1, B7-2, ICOS-L, PD-L1 and PD-L2

74
Q

which TCR leads to inhibition of T cells

A

CTLA-4

75
Q

what is ICOS

A

inducible T cell costimulator

76
Q

what is the effect of ICOS

A

costimulate effector and T reg cells to generate ThF cells

77
Q

homologs of PD-L1

A

B7-H1, CD 274

78
Q

homologs of PD-L2

A

B7-DC, CD 273

79
Q

what cells have PD-1 receptors

A

T cells, B cells, myeloid cells

80
Q

what do PD or program death 1 do

A

negative regulation of T cells

81
Q

what is CTLA 4 a signal for vs. PD1

A

CTLA is stay at this level of activation to not activate more while PD1 is for Apoptosis to complete end all T cell activation

82
Q

what usually activates PD-1

A

tissue aggregation and inflammation

83
Q

when is CTLA 4 induced and where

A

in naive T cells when Ag are initially sensed

84
Q

how do CTLA4 get to surface of T cells

A

stored in intracellular vesicles that are transported to the surface with Ag encounter

85
Q

what regulates CTLA 4 expression

A

greater TCR stimulation means greater CTLA 4

86
Q

what acts as a signal damper and what does this mean

A

CTLA 4 for consistent T cell activation

87
Q

what does PD1 checkpoint work on

A

effector T cells in peripheral tissue to regulate immune response in tissues

88
Q

what causes PD1 expression

A

activated T cells

89
Q

how are PD1 ligands expressed

A

inflammatory signals in tissue cause their expression

90
Q

what does PD-1 do

A

downregulates activity of T cells to limit collateral damage

91
Q

what is most common signal for PDL1

A

IFNy produced from Th1 cells

92
Q

what does too much PDL1 lead to

A

exhausted or anergic state

93
Q

what is a rheostat

A

controls T cell activation such as something that controls electrical current

94
Q

how does PD1 inhibit TCR

A

SHP2 is activated to block ZAP70

95
Q

what is 3rd signal shown with PD-1

A

IFNAR with JAK and TYK2

96
Q

what do JAK and TYK2 induce

A

STAT 1 and 2 With IRF9 for cell growth and survival

97
Q

what do cytokines control when T cells are activated

A

outcome of Ag recognition for effector T cell differentiation: which T cells produced

98
Q

what does IL12 do

A

activates STAT4 for T bet production to cause Th1 cells

99
Q

what activates Th2 cells and how

A

IL4 through STAT6 that leads to expression of GATA 3

100
Q

what causes TH17 production

A

IL6 activates STAT3 which activates RORyt

101
Q

what is RORyt

A

retinoic acid receptor related orphan receptor

102
Q

what activates T reg cells

A

TGFB activates SMAD2 and 4 to activate FOX3 for Treg

103
Q

what signal is cytokine production

A

signal 3

104
Q

what is the first thing produced in CD4+ helper cells after T cell activation

A

C-Fox

105
Q

when are IL2, CD 69, IL2Ra and CD40L produced on activated T helper cells

A

IL2 first at 12 hours, CD 69 at 1day, IL2Ra at 1 day, CD40L at 1.25 days

106
Q

what is IL2R for

A

proliferation

107
Q

what is CD 40 L for

A

activation of dc, macrophages and B cells

108
Q

what is CD 69

A

keeps T cells in lymphoid organs by causing expression of S1PR1

109
Q

what allows activated T cells to exit lymphoid organs

A

CD 69 expression decreases and S1PR1 is re-expressed for exit of effector and memory T cells

110
Q

Cytokine for IL2Ra

A

CD 25

111
Q

what is IL 2

A

autocrine growth factor for CD4+ and CD8+ T cells

112
Q

which cells have cytotoxicity induced by IL2

A

NK cells and CD 8+ T cells

113
Q

what does IL2 cause T cells to produce

A

IL4,5, and IFN y

114
Q

what does IL2 promote the development of

A

regulatory T cells

115
Q

how does IL2 cause death of T cells

A

induces autocrine activation induced death by CTLA 4

116
Q

how does IL2 cause survival of T cells

A

induced antiapoptotic protein Bcl-2

117
Q

how does IL2 induce proliferation

A

stimulates cell cycle progression by degrading cell cycle inhibitor p27

118
Q

what is special about IL2

A

no cytokine can replace it

119
Q

what T cell need IL2 for survival and function

A

Treg

120
Q

which cells besides T cells have proliferation and differentiation stimulated by IL2

A

NK cells and B cells

121
Q

what is S1PR1

A

sphingosine-1 phosphate receptor

122
Q

why is CD 25 expression increased in activated T cells

A

binding of IL2 for proliferation

123
Q

if IL2R doesn’t have an a subunit what occurs

A

IL2 binds but not enough affinity to surpass threshold

124
Q

which ligand expressed on activated T cells

A

CD 40L

125
Q

when is CD40L or CD154 expression increased

A

24 to 48 hours after TCR activation

126
Q

what is the role of CD40L

A

helps DC, macrophages and B cells become better APCs by engaging CD 40 for more expression of B7 (CD80) and cytokines

127
Q

CD 40L is a major inducer of

A

signal 3

128
Q

what is clonal expansion

A

primary recognition of MHC complexes and causes many events

129
Q

what does elimination of Ag lead to

A

contraction of T cell response

130
Q

why does T cell response need to decline

A

maintain homeostasis

131
Q

what drops with decline of T cell response

A

costimulation, IL2, and anti-apoptotic proteins

132
Q

what does IL2 starvation cause

A

mitochondrial pathway of apoptosis

133
Q

what induced apoptosis

A

death receptors TNFRI and FAS

134
Q

what T cell causes contraction of T cell response

A

Treg Cells

135
Q

how can Memory T cells develop

A

from effector cells or directly from naive T cells

136
Q

linear model of memory t cells

A

most effector cells die and those that live become memory

137
Q

Branched, differentiated memory t cells

A

effector and memory cells are alternative fates of activated T cells

138
Q

how do memory t cells survive

A

anti-apoptotic proteins for whole life

139
Q

what is the most abundant lymphocyte population in a person’s life time

A

memory T cells

140
Q

where do memory T cells resides

A

tissue of lymphoids, intestines, lungs, skin for barrier of defense and where Ag first go

141
Q

what influences the development of effector or memory T cells

A

TFs

142
Q

Tbet drives

A

effector cells in CD4+ cells

143
Q

BLIMP1 promotes

A

memory T cells

144
Q

what is last immune response to develop in infants

A

T cell mediated immune response

145
Q

why such a large memory T cell population

A

larger and enhanced response to Ags

146
Q

time for naive T cells vs. memory T cells to respond to Ag

A

naive in 5 to 7 days while memory is 1 to 3 days

147
Q

number of memory vs. naive for Ag

A

memory is 10 - 100x naive

148
Q

where do Memory go for Ag

A

migrate to peripheral tissue to respond

149
Q

what allows memory cell migration

A

adhesion molecules and chemokine receptors

150
Q

what contributes to memory cell long life

A

slow self-renewing

151
Q

what does maintenance of memory cells depend on

A

cytokines but not Ag

152
Q

what induces the expression of Anti-apoptotic for low level proliferation of memory cells

A

IL7 and 15

153
Q

3 phases of memory cells

A

generation, homeostasis and immunosenescence

154
Q

when are memory cells made

A

infancy, youth, young adulthood (0-20)

155
Q

when is homeostasis

A

plateau for 30-65 years old

156
Q

what happens in immuno-senescence

A

after 65, memory cells stop production all together and pathogen susceptibility increases

157
Q

markers of memory T cells

A

IL7R, CD 45, CD 27

158
Q

how are CD 4+ and CD 8 memory T cells divided

A

subsets based on homing and fxn

159
Q

central memory T cells

A

express chemokine receptor CCR7 and L selectins for homing in LN, spleen and blood

160
Q

which type of memory T cells proliferate effector cells and how

A

central memory cells by high IL2 and make many effector cells

161
Q

effector memory cells are found where

A

blood only

162
Q

what do effector memory cells do

A

don’t proliferate but produce IFNy and TNF or become cytotoxic

163
Q

whre are resident memory T cells

A

epithelial barrier tissues

164
Q

what is produced by Trm

A

IFN and TNF for specific pathogens and other Ags encountered previously

immunology (10 decks)

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