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Host Defense > T-Cell Immunity I & II > Flashcards

T-Cell Immunity I & II Flashcards

1
Q

When is the adaptive immune response initiated?

A

when naive T-cells recognize peptide-MHC complex on the surface of APCs; upon TCR signaling, T-cells are activated

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2
Q

Do effector T-cells act on target cells or the pathogens themselves?

A

target cells

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3
Q

What is the cell surface marker of a naive vs. memory T- cell?

A
  • naive: CD45RA

- memory: CD45RO

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4
Q

Which chemokine receptor (CCR) do central vs. effector memory cells contain?

A
  • central: CCR7

- effector: CCR3 and CCR5

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5
Q

Where are effector vs. central memory cells found?

A

effector memory cells (CCR3 and CCR5) rapidly mature into effector cells upon reactivation and migrate into inflamed tissues; central memory cells (CCR7) take longer than effector memory cells in producing cytokines, and they remain in lymphoid tissue

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6
Q

What is another name/designation for CD80/CD86?

A

B7

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7
Q

APCs deliver 3 kinds of signals to naive T-cells:

A
  1. Activation (TCR binds MHC)
  2. Survival (CD28 binds CD80/CD86)
  3. Differentiation (cytokine receptors bind cytokines to determine type of effector T-cell)
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8
Q

What is responsible for dictating the fate of T-cell differentiation into distinct subsets of effector T-cells?

A

cytokines

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9
Q

What is the difference b/t the IL2 receptor that naive T-cells vs. activated T-cells express?

A
  • naive: ILγβ (low-moderate affinity)

- activated: ILγβα (high affinity)

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10
Q

The common gamma chain is expressed in which interleukin types? What is the implication of this?

A

IL2, 5, 7, 9, 15, 21
Because it is found in so many interleukin types, a mutation in the common gamma chain can have very negative consequences, such as severe immune deficiency diseases (SCID).

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11
Q

CD4 helper cell fates depend upon activation of differentiation. Which 2 things are required to activate differentiation of a naive CD4 cell?

A
  1. Specific combination of interleukins/cytokine

2. A transcription factor

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12
Q

Which TF does Th1 require for activation?

A

Tbet

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13
Q

Which TF does iTreg require for activation?

A

FOXP3

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14
Q

Which TF does Thf require for activation?

A

BCL6

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15
Q

Which TF does Th17 require for activation?

A

RORγt

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16
Q

Which TF does Th2 require for activation?

A

GATA3

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17
Q

Effector CD4+ T-cells can be classified by the ______ they produce.

A

signature cytokines

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18
Q

Which signature cytokines do Th1 cells produce?

A

IFNγ, IL2, lymphotoxin-α (LTα)

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19
Q

Which signature cytokines do Th2 cells produce?

A

IL4, IL5, IL6, IL10, IL13

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20
Q

Which signature cytokines do iTreg cells produce?

A

TGFβ, IL10

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21
Q

Which signature cytokines do Th17 cells produce?

A

IL17, IL21, IL22

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22
Q

Which signature cytokines do Thf cells produce?

A

IL4, IL10, IL21

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23
Q

What are Th1 cells involved with?

A
  • quintessential cell type involved in cell-mediated inflammation and delayed-type hypersensitivity rxn
  • targeting intracellular pathogens
  • various autoimmune diseases (self-antigens)
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24
Q

What are Th2 cells involved with?

A
  • targeting extracellular pathogens

- immunopathology of allergies, asthma, dermatitis

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25
Q

What are iTreg cells involved with?

A
  • immune tolerance

- regulation of immune response to self antigens

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26
Q

What are Th17 cells involved with?

A

gut immunity

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27
Q

What are Thf cells involved with?

A

-located in B-cell follicle and assist differentiation of B-cells into memory and plasma cells

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28
Q

Lymphocytes and macrophages use cytokines to do what?

A

regulate the intensity of an immune response

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29
Q

What is the unique function of dendritic cells and macrophages?

A

They uptake pathogens and process bacterial proteins for antigen presentation in the context of self MHC. They can also respond to bacterial products and viral RNA/DNA through Toll-Like Receptors (TLRs).

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30
Q

The immune system protects against 4 classes of pathogens:

A
  1. Extracellular bacteria, parasites, and fungi
  2. Intracellular bacteria and parasites
  3. Viruses (intracellular)
  4. Parasitic worms (extracellular)
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31
Q

TLRs respond to which ligands?

A

PAMPs, DAMPs, MAMPs,

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32
Q

Are TLRs present on the cell surface membrane or the membrane of intracellular vesicles?

A

can be found on both!

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33
Q

What are the APCs that initiate the T helper response?

A

dendritic cells and macrophages

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34
Q

Which are the professional antigen presenting cells, and what are their defining features?

A
  • dendritic cells, macrophages, B-cells

- defining features: MHC I & II, co-stimulatory molecules

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35
Q

What triggers conversion of an immature DC to a mature DC?

A

recognition and uptake of a living pathogen or complex antigen by a DC

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36
Q

What happens when an immature DC becomes a mature one?

A
  • can no longer phagocytose
  • upregulates its MHCII
  • upregulates co-stimulatory molecules (CD80, CD86, CD40)
  • migrates to lymphoid tissue and upregulates production of cytokines
37
Q

What are the antigen presenting cells of the skin?

A

Langerhans cells

38
Q

Which type of dendritic cells stimulate naive T-cells?

A

B7+ (B7+ DCs look for T-cell with corresponding receptor for that particular peptide, leading to expansion/differentiation into other types of T-cells that can help get rid of the pathogen)

39
Q

What is the difference b/t a primary and secondary lymphoid follicle?

A
  • primary: resting and not active

- secondary: active with germinal center

40
Q

Where are T-cells primarily located in the lymph node?

A

paracortical area

41
Q

What are the inducing cytokines for Th1 cells?

A

IL12, IFNγ

42
Q

Describe interferon-gamma (IFNγ).

A
  • potent inflammatory cytokine!
  • signature cytokine of Th1 response
  • also a cytokine of NK cells and activated CD8 cells
  • activates macrophages to incr. release of inflamm. mediators
  • potent suppressor of Th2 and Th17 response
43
Q

IFNγ is a potent suppressor of which T-cell response?

A

Th2 and Th17

44
Q

Describe toll-like receptors.

A
  • class of proteins that play a key role in the innate immune system
  • single pass, membrane-spanning, non-catalytic receptors usually expressed on sentinel cells such as macrophages and dendritic cells
  • recognize structurally-conserved molecules derived from microbes
45
Q

Describe IL2.

A
  • critical growth cytokine produced by activated Th1 and CD8
  • growth factor for Treg cells
  • acts in autocrine and paracrine modes
  • high affinity IL2R expressed after antigen activation on T-cells and expression of CD25 subunit
  • implicated in certain genetic defects
46
Q

Describe lymphotoxin-α

A
  • part of TNF (tumor necrosis factor) family
  • produced by Th1, CD8, NK, B-cells, macrophages
  • implicated in immunopathology of rheumatoid arthritis and disease progression of MS
47
Q

What is the classic tetrad of pro-inflammatory cytokines produced by a macrophage?

A

IL1, IL6, IL8, and TNF-α

These cytokines have a wide range of autocrine, paracrine, and systemic effects that promote inflammation.

48
Q

Describe IL1.

A
  • primordial pro-inflammatory cytokine
  • facilitates host response to stress
  • produced by a wide range of cell types, including epithelial cells
  • promotes neutrophil growth and emigration from BM
  • acts w/ IL6 on CNS to cause fever and depression
  • antagonist is IL-1Ra
  • acts w/ TGF-beta, IL6, IL21, and IL23 to induce differentiation of Th17
49
Q

Describe IL6.

A
  • pro-inflammatory cytokine
  • many effects redundant w/ IL1 (fever, induction of acute phase protein)
  • promotes responsiveness to IL2
  • required for optimal Th17 development
  • has effects on bone mineral metabolism, where it activates osteoclasts
50
Q

Describe IL8.

A
  • most potent stimulus for mobilizing/recruiting neutrophils to site of infection (chemotactic activity)
  • produced mainly by macrophages, neutrophils, and during intense inflamm. by endothelial cells (drives edema response)
51
Q

Describe TNF-α.

A
  • pro-inflammatory cytokine/cytotoxin
  • potent macrophage activator
  • potent upregulator of MHC and other cytokines
  • potent inducer of angiogenesis! (and potentially apoptosis)
  • causes local tissue destruction
  • availability of anti-TNF antibody implicated in treatment of inflammatory diseases
52
Q

What is hypersensitivity reaction type IV?

A
  • delayed-type hypersensitivity
  • mediated by antigen-specific effector Th1 cells and CD8 cytotoxic T-cells
  • commonly applied to clinical situations where macrophage activation is central component of disease pathology
  • can be exploited for tuberculin test to detect past infections
53
Q

What are the inducing cytokines for Th2?

A

IL4

54
Q

What are the characteristics of a Th2 response?

A

Any infection or antigenic stimulus that causes dominant production of IL4 by the activated T-cells:

  • soluble antigen
  • bacterial
  • multi-cellular parasites
55
Q

What is the function of the Th2 cytokine, IL4?

A
  • absolute requirement for Th2 response (growth factor for Th2 and also produced by Th2)
  • promotes B-cell growth and induces B-cells to differentiate into Ab-producing plasma cells
  • induces class switching from IgG to IgE (therefore, plays a role in allergies)
  • inhibits development of Th1 on T-cells
  • inhibits Th-1 mediated macrophage activation (therefore, it is anti-inflammatory)
56
Q

Is IL4 anti- or pro-inflammatory?

A

anti-inflammatory

57
Q

How to T-cells facilitate B-cell differentiation?

A

Antigen recognition (antigen is on B-cell surface and recognized by T-cell) induces expression of effector molecules (like cytokines) by the T-cell, which leads to activation of the B-cell.

58
Q

How is the Th2 response related to B-cells?

A

Th2 enhances B-cell function and ultimately antibody production by making pathogens more attractive to macrophages, binding toxins, and targeting mutant/virus-infected cells for killing.

59
Q

Aside from IL4, what are the other Th2 cytokines and their major functions?

A
  • IL5: role in eosinophil maturation, drives allergic type inflammatory response and promotes pathology of Th2-mediated immune diseases
  • IL13: also has a role in allergic type inflammatory response and promotes pathology of Th2-mediated immune diseases
  • IL10: major driver of B-cell differentiation and isotype switching, also produced by iTreg and Thf, inhibits Th1 differentiation and DC function (so, inhibits production of pro-inflammatory cytokines)
60
Q

What are the inducing cytokines for Th17 cells?

A

TGFβ (IL1), IL6, IL21, IL23

61
Q

What is the major function of Th17?

A

It is inflammatory and involved in organ-specific autoimmune diseases like MS, type I diabetes, IBD, and airway inflammatory disease. It produces multiple types of IL17, which is involved with recruitment/activation of neutrophils and monoctyes and expression of pro-inflammatory cytokines IL6 and IL8.

62
Q

What is the function of IL21?

A
  • produced by Th17
  • enhances B-cell function
  • contributes to Ab-mediated pathology like hyper IgE syndrome (which causes recurrent staph and fungal infections)
63
Q

What is the function of IL22?

A
  • produced by Th17
  • functions in protective immunity of gut by restricting commensal bacteria to their niches
  • induces expression of antimicrobial peptides
64
Q

Which differentiated T-cells share IL10?

A

iTreg, Thf, and Th2

65
Q

What are the main functions of Thf cells?

A
  • T follicular helper T-cells facilitate humoral immune responses by assisting B-lymphocytes with production of pathogen-neutralizing antibodies
  • found in B-cell zone of secondary lymphoid organ (ie, lymph nodes)
  • recruitment to B-cell zone mediated by chemokine receptor, CXCR5
  • fully mature Thfs found in germinal center upon interacting w/ B-cells
66
Q

Which things are critical for the development of Thf cells?

A

transcription factor BCL6, IL6, IL21, and CXCR5 chemokine receptor

67
Q

After a functional Thf leaves the paracortical region and migrates to the primary follicle of the lymph node, what happens?

A

The Thf will migrate into the secondary follicle with a germinal center. Functional Thf makes IL4, IL10, and IL21, which all act on B-cells and induce them to differentiate into plasma cells.

68
Q

Which interleukins are involved with B-cell survival vs. class switching?

A
  • B-cell survival: IL4, IL10

- Ig class switching: IL4, IL10, IL21

69
Q

What are the inducing cytokines for iTreg cells?

A

TFGβ (IL1) and IL2

70
Q

What are the 2 types of CD4 Treg cells?

A
  • natural Treg (nTreg): developed in thymus from DP thymocytes
  • induced Treg (iTreg): developed in peripheral lymphoid tissues
71
Q

What happens when there is a mutation in FOXP3?

A

IPEX (an autoimmune disorder)

72
Q

What are the 2 mechanisms of suppression that Treg carries out?

A

1) Cell-cell contact: involves inhibitory receptors
2) IL10: acts on APCs to reduce expression of MHCII and co-stimulatory molecules CD80/86, reduces release of pro-inflammatory cytokines by mast cells, important in IBD and colitis

73
Q

What are the main functions of Treg cells?

A
  • play a critical role in maintenance self-tolerance
  • regulate immune responses
  • important in IBD and colitis
74
Q

What are the 3 phases of the CTL response?

A

1) Effector phase: 1-2 days after acute infection
2) Contracting phase: once source of infection is eliminated, most CTL die by apoptosis and only 5-10% survive
3) Memory phase: surviving 5-10% establish memory pool (can last up to 75 years in humans)

75
Q

Where does initial activation of naive CD8 occur?

A

in the peripheral region near the marginal sinus, where naive CD8 and DC migrate from the deeper T-cell zone of the paracortical region

76
Q

What are the human diseases involved with TCRγδ?

A
  • HIV infection: incr. in freq. of TCRδ1, decr. in TCRδ2
  • Tb: pts w/ active Tb decr. TCRγδ; healthy contacts incr. TCRγδ
  • Parasitic infection: malaria incr. TCRδ1
77
Q

What is meant by TCRγδ having a restricted repertoire?

A

They only have 3 Vδ and 7Vγ because only a few of the genes undergo rearrangement.

78
Q

How are antigens presented to TCRγδ receptors?

A

They are NOT presented by MHC I or II, but by CD1b, CD1c, and CD1d.

79
Q

Are antigens presented to TCRγδ receptors peptides?

A

No, they are phospholipids or phosphoantigens.

80
Q

Where are TCRδ1 vs. TCRδ2 found?

A
  • TCRδ1: mucosal tissue; associated w/ epithelial cell functions
  • TCRδ2: circulation; majority generated in fetal liver (but some generated in thymus)
81
Q

What are the 3 main mechanisms of killing for CTLs?

A

1) Contact-mediated cytolytic effect
2) FAS-FASL mediated apoptosis (leads to activation of caspase 8 that induces MT damage and eventually DNA fragmentation)
3) Cytotoxic granules or lysosomes (perforin, granzyme B, granulysin)

82
Q

How to T-cells deliver cytotoxic granules to target cells?

A

Recognition of the target cell causes redistribution of the cytoskeleton and cytoplasmic components of the T-cell, causing release of cytotoxic granules at the site of cell contact. So, in essence, the T-cell must mobilize the granules toward the target cell to most effectively kill it.

83
Q

Which cytokine enhances the synapse formation between CTLs and target cells?

A

IL12

84
Q

What is the T-cell growth factor for most T-cells?

A

IL2

85
Q

Which cytokine has chemotactic activity and is the most potent stimulus for mobilizing/recruiting neutrophils to the site of infection?

A

IL8

86
Q

How does the Th2 response enhance B cell function?

A
  • makes pathogens more attractive to macrophages
  • binds toxins
  • targets mutant/viral-infected cells for killing
87
Q

Which cytokine is a potent regulator of class switching?

A

IL4

88
Q

Why can IL4 be considered an anti-inflammatory cytokine?

A

It inhibits the Th1-mediated macrophage activation.

89
Q

Stimulation of APC through CD40 increases _____ and _____, which co-stimulate the naive CD8 T-cell and help it mature into a functional cytotoxic T-cell.

A

B7; 4-IBBL

Host Defense (24 decks)

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