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HDM Final > Cytotoxic Cell-mediated Immune Response > Flashcards

Cytotoxic Cell-mediated Immune Response Flashcards

1
Q

What identifiers are expressed on resting mature naive T cells?

A 
CD4 or CD8
CD28
HLA class I
TCR complex with CD3
LFA-1 and VLA-4 adhesion molecules
Chemokine receptors
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2
Q

Mature naive T cells express CD28, what is this a receptor for?

A

CD80 (B7-1) and CD86 (B7-2)

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3
Q

What is the only constitutively expressed B7 receptor on naive T cells?

A

CD28

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4
Q

What is the result if a TCR binds an APC without CD28:B7 interaction?

A

Anergy

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5
Q

Where are naive T cell responses initiated?

A

Peripheral lymphoid organs, like LNs

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6
Q

Innate immune responses aid in initiation of T cell activation through generation of inflammation. What cell type ALONE is capable of activating naive T cells?

A

Dendritic cells

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7
Q

If only DCs can activate naive T cells, what are the roles of B cells and macrophages as APCs in the adaptive immune response?

A

B cells and macrophages activate memory T cells

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8
Q

What cells are responsible for activating the B cells and macrophages that can then activate CTLs?

A

CD4 T cells

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9
Q

Naive T cell activation begins when they enter the LN via ___________ in the cortex

A

High endothelial venules

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10
Q

Once the naive T cell has crossed the high endothelial venule in the cortex of the LN, what happens if it does not encounter a specific Ag?

A

It will leave the LN through efferent lymphatics

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11
Q

Once in the LN, naive T cells monitor antigen presentation by what 2 cell types?

A

Macrophages

Dendritic cells

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12
Q

T cells that encounter specific antigen proliferate and differentiate to effector cells, resulting in cytokine production.

Which type of T cells increases to the greater degree upon Ag recognition?

A

CD8+ T cells increase more

[CD4 increase 100-1000x, while CD8 increase 100,000x]

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13
Q

Within ____ days of antigen appearing in a LN, it has been bound by its naive antigen specific T cell

____ days after the arrival of Ag, activated effector cells emigrate from the LN into periphery

A

2

5

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14
Q

What is the primary function of CD3 in the TCR-APC immunological synapse?

A

Signal transduction by TCR complex

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15
Q

What is the primary function of zeta chains in the TCR-APC immunological synapse?

A

Signal transduction by TCR complex

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16
Q

What is the primary function of CD4 in the TCR-APC immunological synapse, and what is its ligand?

A

Signal transduction (coreceptor, stabilization)

Ligand: Class II HLA (on APC)

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17
Q

What is the primary function of CD8 in the TCR-APC immunological synapse, and what is its ligand?

A

Signal transduction (coreceptor, stabilizing)

Ligand: Class I HLA (on APCs and CTL targeting cells)

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18
Q

What is the primary function of CD28 in the TCR-APC immunological synapse, and what is its ligand?

A

Signal transduction (costimulation)

Ligand: B7-1/B7-2 (on APC)

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19
Q

What is the primary function of CTLA-4 in the TCR-APC immunological synapse, and what is its ligand?

A

Signal attenuation

Ligand: B7-1/B7-2 (on APCs)

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20
Q

What is the primary function of LFA-1 in the TCR-APC immunological synapse, and what is its ligand?

A

Adhesion

Ligand: ICAM-1 (on APCs and endothelium)

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21
Q

What is the primary function of VLA-4 in the TCR-APC immunological synapse, and what is its ligand?

A

Adhesion

Ligand: VCAM-1 (on endothelium)

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22
Q

What term is used interchangeably for B7-1/B7-2?

A

CD80

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23
Q

What is the general T cell activation pathway?

A

Formation of synapse

Activation of 2 tyrosine kinases:
1. Fyn –> phosphorylation of ITAMs of CD3 and zeta chains

  1. Lyk (src family) –> phosphorylates and activates tyrosine kinase ZAP-70 associated with zeta chain
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24
Q

PLC activation leads to two potential transcription factors, NFAT and NFkB. How does PLC activation lead to NFAT?

A

Increased cytosolic Ca2+ –> calcineurin –> NFAT

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25
Q

PLC activation leads to two potential transcription factors, NFAT and NFkB. How does PLC activation lead to NFkB?

A

DAG –> PKC –> NFkB

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26
Q

How does T cell activation lead to AP-1 transcription?

A

Via Ras-MAPK pathway, production of RasGTP and ERK, JNK

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27
Q

In addition to LFA-1 and VLA-4, what else is present on the T cell mediating adhesion in the immunological synapse?

A

CD2 (binds LFA-3 ligand on APC)

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28
Q

When a T cell first recognizes antigen presented by an APC, there is weak adhesion and NO T cell response. What changes occur in order to generate a stronger interaction?

A

APC releases chemokines that activate integrins on the T cell surface –> the integrins will cluster together and increase their affinity (via conformational change), leading to strong adhesion and a T cell response

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29
Q

What process is often necessary for full CD8 T cell activation?

A

Cross-presentation

both CD4 and CD8 bind to DC presenting antigen. CD4 will release cytokines to the CD8 cell to help activate it

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30
Q

Activation of T cells triggers a cascade of protein production.

Once change involves increase in ______ expression on T cells, which interacts with a receptor on APCs to strengthen adhesion, hence prolonging T cell-APC contact

A

CD40L (binds CD40 on APCs)

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31
Q

Activation of T cells triggers a cascade of protein production.

What transcription factors are likely to be produced in response to T cell activation?

A

c-Fos

c-Myc

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32
Q

Activation of T cells triggers a cascade of protein production.

What membrane effector molecules are likely to be upregulated during T cell activation?

A

CD40 ligand

Fas ligand

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33
Q

Activation of T cells triggers a cascade of protein production.

What cytokines are likely to be secreted during the T cell activation process?

A

IL-2
IFN-y
IL-4

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34
Q

Activation of T cells triggers a cascade of protein production.

What cytokine receptors are likely to be upregulated during the process of T cell activation?

A

IL-2R

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35
Q

There are several cytokines produced by T cells once they are activated. What is the principle action and cellular source of IL-2?

A

Survival, proliferation, differentiation of effector and regulatory T cells

Source: CD4 and CD8 T cells

36
Q

There are several cytokines produced by T cells once they are activated. What is the principle action and cellular source of IL-4?

A

B cell switching to IgE

Source: CD4 T cells, mast cells

37
Q

There are several cytokines produced by T cells once they are activated. What is the principle action and cellular source of IL-5?

A

Activation of eosinophils

Source: CD4 T cells, mast cells

38
Q

There are several cytokines produced by T cells once they are activated. What is the principle action and cellular source of IFN-y?

A

Activation of macrophages

Source: CD4 and CD8 T cells, NK cells

39
Q

There are several cytokines produced by T cells once they are activated. What is the principle action and cellular source of TGF-beta and IL-10?

A

Inhibition of T cell activation; differentiation of Treg cells

Source: CD4 regulatory T cells; many other cell types

40
Q

What type of signal is IL-2?

A

Autocrine

41
Q

Describe the expression and affinity of IL-2R on T cells.

A

IL-2R is constitutively expressed as a low affinity receptor

Binding of IL-2 leads to expression of IL-2Ralpha chain, which forms HIGH affinity complex

Binding of IL-2 to high affinity IL-2R promotes T cell proliferation and differentiation

42
Q

Which cytokines, present at the site of infection, cause the naive CD4 cell to switch to Th1?

A

IFN-y

IL-12

43
Q

Which cytokines, present at the site of infection, cause the naive CD4 cell to switch to Th2?

A

IL-4

44
Q

Which cytokines, present at the site of infection, cause the naive CD4 cell to switch to Th17?

A

TGF-beta
IL-6
IL-23

45
Q

Th1 cells are characterized by IFN-y secretion. What 3 functions does this cytokine perform when released from Th1?

A

Activates macrophages

Activates B cells to stimulate complement binding

Stimulates class II HLA and CD80 on B cells

46
Q

Other than IFN-y, what cytokine does Th1 produce?

A

TNF-alpha

47
Q

What cytokines are released from Th2 cells?

A

IL-4
IL-13
IL-5

48
Q

Th17 cells release several cytokines, but which one is considered characteristic of Th17 cells?

A

IL-17

49
Q

What are the 2 primary functions of IL-17 released from Th17 cells?

A

Barrier function

Neutrophil activation

50
Q

How do bacterial superantigens differ from typical antigens in their activation of T cells?

A

Bacterial superantigens can activate T cells in the absence of co-receptors and co-stimulation

51
Q

Where does a bacterial superantigen bind in the TCR-APC complex?

A

Alpha chain of MHC class II

V-beta region of TCR

52
Q

Where does a viral superantigen bind in the TCR-APC complex?

A

Beta chain of MHC class II

V-beta region of TCR

53
Q

What are some of the consequences of superantigen activation?

A

Fever, rash

Edema, hypotension, shock –> multiple organ failure

54
Q

What 2 cytokines are primarily responsible for multiple organ failure during superantigen activation? How do they do this?

A

TNF-alpha and IL-1

These contribute to an increase in vascular permeability that leads to leakage of fluid from the intravascular space into the perivasculature

55
Q

What is the major difference between effector T cells and resting naive T cells?

A

An effector T cell is able to respond to specific antigen without the need for costimulation via CD80-CD28 interaction

56
Q

During T cell activation, where do antigen recognition, proliferation, and differentiation take place?

A

In the lymph nodes

57
Q

How do activated effector cells travel to the site of infection?

A

In the blood

58
Q

After activation by APCs in the ________ area, CD4+ Th cells change their chemokine receptor expression and migrate to the edge of the _________ zone.

Activated Th cells secrete low levels of cytokines and increase expression of co-stimulatory molecules; eventually they will start expressing _______

A

Medullary; follicular

CTLA-4

59
Q

How do the Th cell chemokine receptors change in order to cause migration of activated T cells to the edge of the follicle?

A

Decreased expression of CCR7

Increased expression of CXCR5

[note that B cells in the B cell zone will upregulate CCR7 to move toward T cell zone]

60
Q

What general effect do interferons have on cytotoxic T lymphocytes ability to kill?

A

They increase HLA expression for T cell recognition

61
Q

True or false: the host cell must be killed in order to eliminate an intracellular pathogen via CTLs

A

True

Stored lytic granules that contain cytotoxins are released directly onto the surface of the infected target cell (perforin + granzymes)

62
Q

What are the 2 mechanisms of CTL killing?

A

Granular proteins (perforin and granzymes)

FasL and Fas (CD95)

63
Q

What do the granular enzymes released by CTLs do to target cells?

A

Perforin forms pore necessary for delivery of granzymes

Granzymes activate caspases in cytosol –> apoptosis

64
Q

What is the Fas/FasL mechanism for CTL killing?

A

Activated CTLs express FasL which binds death receptor Fas on target cells. This interaction results in activation of caspases and apoptosis

65
Q

How does cooperation exist between CD4 and CD8 T cells?

A

CD4 cells release IFN-y, causing killing of microbes in phagolysosome of phagocyte

CD8 then comes in and kills the entire infected cell

66
Q

What cytokines enhance NK cell killing?

A

IFN-alpha
IFN-beta
IL-12

67
Q

What inhibits NK cell killing?

A

MHC class I binding inhibitory receptor

68
Q

What cell markers are found on NK cells?

A

CD16

CD56

69
Q

What intracellular signaling event prevents activation of NK cell killing when the inhibitory receptor is engaged by MHC I?

A

Removal of phosphates from the PTK just inside the membrane

70
Q

ADCC involves what 5 cell types?

A

NK cells
Macrophages
Neutrophils
Eosinophils

71
Q

ADCC involves target recognition through which Ab?

A

IgG

72
Q

What are the killing components of ADCC?

A

Lytic enzymes
TNF
Perforin/granzymes

73
Q

With chronic infection, the viral load remains somewhat constant and CTLA-4 is continuously upregulated. This eventually leads to Th cell ____________

A

Exhaustion

74
Q

What two cellular components are upregulated in chronic infection induced CD8 T cell exhaustion?

A

CTLA-4 (binds B7 on target)

PD-1 (binds PD-1L on target)

75
Q

What happens to most of the effector cells generated in response to a specfic antigen once that infection has been cleared?

A

They are short-lived. Only some become memory T cells.

76
Q

What do memory CD4 and CD8 T cells require to regain their effector functions?

A

They require reactivation, as well as IL-7 and IL-15 for survival

77
Q

What allows our bodies to react much more quickly to secondary infection?

A

Memory T cells do not need coactivators to respond, so they are able to quickly kill the pathogen on secondary infection

78
Q

Is CTLA-4 expression on Treg cells inducible or constitutive?

A

Constitutive

Treg cells constitutively express CD4, CD25, and CTLA-4

79
Q

What is the unique TF associated with Treg cells?

A

FOXp3

80
Q

Tregs express CTLA-4, what does this bind to and what does that cause?

A

CTLA-4 binds CD28 and shuts down IL-2 production

81
Q

Which binds more avidly to CD28: CD80 or CTLA-4?

A

CTLA-4 binds more avidly to CD28

82
Q

PD-1 is a regulatory receptor that is inducible on what cell types?

A

T cells
B cells
myeloid cells

This causes negative regulation of T cells

83
Q

What receptor is inducible on T cells and operates as a costimulator as well as in generation of follicular helper T cells?

A

ICOS

Binds ICOS-L on DCs, macrophages, B cells, and others

84
Q

What cytokine-related evasion mechanism is used by EBV to avoid our immune response?

A

EBV makes an analog of IL-10 leading to inhibition of macrophage and DC activation

85
Q

What type of bacteria evade our immune system by inhibiting phagolysosome fusion?

A

Mycobacteria - they are able to survive within the phagosome

86
Q

What type of pathogen evades our immune system by inhibiting antigen presentation?

A

HSV (inhibits TAP)

CMV (removal of MHC I from ER, inhibits proteosome)

EBV (inhibits proteosome)

87
Q

What type of pathogen evades our immune system by blocking cytokine activation of effector cells?

A

Pox viruses - they produce soluble cytokine receptors that take up any cytokines around so that they cannot bind to receptors on effector cells

HDM Final (12 decks)

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