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I&I SC1 > Advanced immunology > Flashcards

Advanced immunology Flashcards

Lectures: -Week 3, day 4, lecture 1: Advanced lectures - Innate lymphocytes -Week 3, day 4, lecture 2: Advanced lectures - NK-cells -Week 3, day 4, lecture 3: Advanced lectures - Regulatory T-cells

1
Q

Which 3 important B- and T-cell interactions take place in the lymph node?

A
  1. TCR <-> MHCII
  2. C40 <-> CD40L
  3. Cytokines
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2
Q

What additional signal do T-cells give to B-cells which have been activated through their BCR?

A

CD40/CD40L

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3
Q

Which mechanisms allow B-cells to be activated independent of T-cells?

A
  1. Crosslinking of BCR’s by repetitive antigens
  2. TLR’s
  3. BAFF
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4
Q

What is the difference between a T-cell dependent and T-cell independent response?

A
  1. A T-cell dependent B-cell response leads to
    -Extrafollicular response: the formation of plasma cells that produce IgM
    -B-cells that undero the germinal centre reaction, resulting in B-cells with a higher affinity:
    –Non-IgM plasma cells (class switch)
    –Memory B-cells
  2. A T-cell independent B-cell response solely leads to the formation of IgM-producing plasma cells, without affinity maturation, class switch recombination or formation of memory B-cells
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5
Q

What is the approximate response time of an adaptive B-cell response?

A

~10 days

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6
Q

Which types of innate-like lymphocytes can be identified? (4)

A
  1. NK T-cells
  2. B1-cells
  3. γδ-T cells
  4. Marginal zone B-cells
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7
Q

Where do innate-like lymphocytes typically occur?

A

Anatomical locations contacting the outside world, such as mucosal surfaces and the pleural & peritoneal cavity

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8
Q

What is special about the TCR/BCR repertoire of innate-like lymphocytes?

A

They have a very limited receptor repertoire

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9
Q

Do innate-like lymphocytes have TCR/BCR’s?

A

Yes, but with a limited diversity

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10
Q

Why can innate-like B-cells always respond independent of T-cells?

A

They are present in a pre-activated state, only requiring BCR activation to become active

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11
Q

Which types of innate lymphoid cells can be identified? (4)

A
  1. ILC1
  2. ILC2
  3. ILC3
  4. NK-cells
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12
Q

Where do innate lymphoid cells typically occur?

A

Anatomical locations contacting the outside world, such as mucosal surfaces and the skin

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13
Q

Do innate lymphoid cells have a TCR/BCR?

A

No, they don’t

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14
Q

How are innate lymphoid cells activated?

A

By cytokines in their surrounding

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15
Q

Which two types of innate-like B-cells can be identified?

A
  1. Marginal zone B-cells
  2. B1-cells
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16
Q

Where do B1-cells occur?

A

In the peritoneum and pleural cavity

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17
Q

Where do marginal zone B-cells reside? Why is this location advantageous?

A

In the marginal zone of follicles in the white pulp in the spleen; this location is advantageous because they directly contact blood flowing along the follicles in sinuses, allowing them to rapidly respond to sepsis

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18
Q

How are marginal zone B-cells activated?

A

Marginal B-cells are already pre-activated and require relatively little stimulation; this stimulation is provided by repetitive patterns on bacterial antigens encountered during sepsis

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19
Q

Which type of antibody is produced by marginal zone B-cells, and why?

A

IgM, because these cells never undergo a germinal centre reaction and thus never undergo class switch recombination

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20
Q

What are natural antibodies?

A

Natural antibodies are a ‘first line of defence’, produced by B1-cells without prior experience to antigens

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21
Q

What is an important example of natural antibodies, and why?

A

Blood group antibodies, because they prevent blood transfusion to persons with a different blood group

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22
Q

What kind of groups are natural antibodies targeted at? Why is this advantageous?

A

Non-protein antigens such as glycolipids & carbohydrates; these are often found on bacteria

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23
Q

How are B1-cells selected? How does this help them in their function?

A

They are selected on the basis of low-level autoreactivity; this is not harmful to the body, but does cause them to continuously produce antibodies

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24
Q

True or false: in a healthy individual, antibodies produced by ‘regular B-cells’ (non-B1) are in the majority

A

False; in a healthy individual, the continuous production of antibodies by B1-cells is responsible for the majority of the antibodies in the serum

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25
Q

True or false: the natural antibody titre increases during an infection

A

False; the titre of natural antibodies is more ore less constant

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26
Q

How is the limited BCR repertoire of MZ-B-cells and B1-cells achieved?

A

Some V(heavy chain)’s are restricted to specific V(light chains) -> semi-invariant receptors

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27
Q

What is an important compound, commonly found throughout the body, that is responsible for positive selection of MZ-B-cells & B1-cells?

A

Phosphatidylcholine (PtC)

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28
Q

What happens to MZ-B-cells/B1-cells that don’t recognize PtC?

A

They lack the signal needed for positive selection and undergo apoptosis

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29
Q

What kind of antigen do NK T-cells recognize? Which receptor do they use?

A

Glycolipids, recognized through CD1

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30
Q

How are NK T-cells activated?

A

Through the TCR

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31
Q

What is the primary location of NK T-cells?

A

Peripheral tissues

32
Q

What are the main functions of NK T-cells? (2)

A
  1. Cytokine production
  2. Defence against mycobacteria
33
Q

True or false: NK T-cells have a limited receptor repertoire

A

True; they have an invariant alpha-chain and a limited subset of beta-chains

34
Q

Where are γδ-T cells produced?

A

The embryonic thymus

35
Q

What is the primary location of γδ-T cells?

A

Epithelial tissues

36
Q

What are the main functions of γδ-T cells? (2)

A
  1. Cytotoxicity
  2. Immune regulation
37
Q

On the basis of which markers can innate lymphoid cells be identified?

A

Lineage(neg), CD45(pos)

38
Q

True or false: innate lymphoid cells have a TCR/BCR

A

False; they don’t have such a receptor

39
Q

How are ILC’s activated?

A

Through cytokines, specifically IL-7

40
Q

What do ILC’s do when activated?

A

Produce a large amount of cytokines upon activation

41
Q

To which type of cells are ILC1’s analogous?

A

Th1-cells -> cause macrophage activation and oxygen radicals through secretion of IFN-γ

42
Q

Which transcription factor can be found in both ILC1’s and Th1-cells?

43
Q

To which type of cells are ILC2’s analogous?

A

Th2-cells -> secrete IL-4, IL-5 & IL-13, important for extracellular matrix/tissue repair, but also in allergy

44
Q

Which transcription factor can be found in both ILC2’s and Th2-cells?

45
Q

To which type of cells are ILC3’s analogous?

A

Th17-cells -> produce IL-17, IL-22, important for phagocytosis & epithelium survival

46
Q

Which transcription factor can be found both in ILC3’s and Th17-cells?

47
Q

How are ILC2’s activated?

A

Alarmins, which get released when epithelium gets damaged

48
Q

In which way are ILC2’s an example of neuro-immuno interaction?

A

They are controlled by neurotransmitters

49
Q

What are the two general functions of ILC’s?

A
  1. Tissue homeostasis
  2. Rapid responses through the production of cytokines
50
Q

What is the main activator of NK-cells?

51
Q

What are the three main functions of NK-cells?

A
  1. Rapid killing of virus-infected, stressed & malignant cells
  2. Rapid pro-inflammatory cytokine production
  3. Regulators of immune responses
52
Q

What is the process of release of granzyme/perforin granules? (3)

A
  1. Granules containing granzyme/perforin are present in the cytoplasm
  2. Granules get moved to the site of the target cell by microtubule transport
  3. Exocytosis of granules
53
Q

What is the function of perforin and what is the function of granzyme in perforin/granzyme cytotoxicity?

A

Perforin produces pores in the membrane of target cells, allowing granzyme to enter and activate apoptosis pathways

54
Q

True or false: all cells of the immune system use the same granzyme

A

False; there are multiple kinds of granzyme
NK-cells make use of the highest amount of different granzymes

55
Q

In addition to killing by cytokines, which other ways do NK-cells have for cytotoxic effects?

A

Receptor-ligand interactions, such as:
1. FAS/FASL
2. TRAIL/TRAILR

56
Q

What is ADCC?

A

Antibody-dependent cell-mediated cytotoxicity

57
Q

How do NK-cells recognize cells that are marked for cytotoxicity by antibodies? How do they differentiate between cells with low and cells with high levels of antibody?

A

They recognize the FC-tails of IgG using FC-γRIII (CD16); CD16 has a higher affinity for multimeric IgG, which occurs in antigen-antibody complexes or when IgG is bound to a cell

58
Q

Which cytokines are produced in high levels by NK-cells? (2)

A
  1. IFN-γ
  2. TNF-α
59
Q

How do NK-cells interact with macrophages?

A

At the start of infection, NK-cells are activated by cytokines produced by macrophages (IL-12, IL-18)
They then produce cytokines that activate more macrophages (GM-CSF, TNF-α)

60
Q

Which four reasons cause NK-cells to be classed as innate immune cells?

A
  1. Rapid responses without clonal expansion/differentiation into effector cells
  2. No antigen-specific receptor that requires gene rearrangement
  3. Ready-to-use germline-encoded inhibitory & activating receptors that are reduced on stresses/infected/malignant cells
  4. No formation of memory cells with higher affinity after activation
61
Q

What are the common markers for NK-cells?

A

CD3- & CD56+

62
Q

Which two subsets of NK-cells can be identified?

A
  1. CD56(bright)
  2. CD56(dim)
63
Q

Which are in the majority in the blood: CD56(bright) or CD56(dim) NK-cells?

A

CD56(dim) NK-cells form ~90% of NK-cells found in the blood

64
Q

Which are in the majority in the lymph nodes: CD56(bright) or CD56(dim) NK-cells?

A

CD56(bright) NK-cells form ~75% of NK-cells in the lymph nodes

65
Q

Which NK-cells are the Iargest NK-population in the body: CD56(bright) or CD56(dim) NK-cells?

A

CD56(dim) form 90% of the total NK-cells in the body

66
Q

What are the characteristics of CD56(bright) vs CD56(dim) NK-cells? (4)

A
  1. Cytotoxicity is higher in CD56(dim) than in CD56(bright) NK-cells
  2. ADCC is higher in CD56(dim) than in CD56(bright) NK-cells
  3. CD56(dim) cells have a slower cytokine production than CD56(bright) cells
  4. CD56(bright) cells modulate APC’s using cytokines, whereas CD56(dim) cells are responsible for tissue surveillance for virus-infectes/stressed/malignant cells
67
Q

How do NK-cells recognize which cells are healthy and which cells are diseased?

A

NK-cells are switched off when they encounter a healthy cell, because these cells express inhibitory singals

68
Q

What is a cue that causes NK-cells to identify ‘missing self’? Why is this advantageous?

A

NK-cells are activated when the encounter cells with low/no MHCI-expression
This is advantageous because both viruses and tumours often downregulate MHCI to prevent CD8+ T-cell responses -> NK-cells are still able to identify and kill these cells

69
Q

What are KIR-molecules?

A

Killer immunoglobulin-like receptors; inhibitory & activating receptors found on NK-cells

70
Q

What do KIR-molecules recognize?

A

Specific motifs on MHC-molecules

71
Q

Why is there a large array of KIR-molecules?

A

Because they recognize specific motifs on MHC-molecules, and because MHC-molecules are highly diverse (within the population), there also needs to be a wide variety of KIR-molecules

72
Q

KIR-L’s are often [inhibitory/activating]. How can this be identified intracellularly?

A

Inhibitory; have a large intracellular domain

73
Q

KIR-S’s are often [inhibitory/activating]. How can this be identified intracellularly?

A

Activating; have a small intracellular domain

74
Q

How can NK-cells dampen immune responses?

A

Lysis of activated T-cells to downregulate the immune response

75
Q

How can NK-cells have immune memory? How do they respond differently from ‘normal’ NK-cells? (4)

A

Recurrent infection leads to expansion of virus-specific NK-cells
Response:
1. Stronger ADCC
2. Higher cytokine release
3. Lower response to IL-12/IL-18
4. Possibly lower T-cell regulation

I&I SC1 (20 decks)

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