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𝓘𝓂𝓂𝓊𝓃𝑜𝓁𝑜𝑔𝓎 > Natural Killer and Cytotoxic T Cells > Flashcards

Natural Killer and Cytotoxic T Cells Flashcards

1
Q

What is the difference between innate and adaptive immune responses?

A

➝ innate : non-specific, immediate response

➝ Adaptive : highly-specific, delayed

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2
Q

Where do NK and T cells arise from?

A

➝ common lymphoid progenitor

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3
Q

What kind of cells are NK cells?

A

➝ innate lymphoid cells

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4
Q

What is the role of cytotoxic lymphocytes?

A

➝ kill cells infected with bacteria, viruses or parasites

➝ kill tumor cells

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5
Q

Where are MHC proteins found and what do they do?

A

➝ at the cell surface

➝ form a structure that holds antigenic peptides for surveillance

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6
Q

What cell is MHC I recognised by?

A

➝ CD8+ cytotoxic T cells

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7
Q

What proteins does MHC I present?

A

➝ ALl proteins including normal cellular proteins and not just viral

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8
Q

How is does MHC present intracellular proteins?

A

➝ they are cleaved by the proteasome
➝ transported into the ER
➝ bind to MHC I
➝ transported to the cell surface

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9
Q

How does an infected cell get killed by CD8+ T cells?

A

➝ viruses infect cells
➝ viral proteins are synthesized in the cytoplasm
➝ peptide fragments are bound to MHC class I
➝ MHC presents the viral peptides to the surface
➝ Cytotoxic T cells recognise viral peptides and kill the infected cells

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10
Q

What is the structure of MHC class I?

A

➝ Two polypeptides not covalently bound

➝ alpha 3 domain and beta 2 microglobulin are there to provide support to the peptide binding groove

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11
Q

Why haven’t pathogens mutated to avoid MHC presentation?

A 
➝ There are multiple genes of MHC class I 
➝ high genetic variability within these genes
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12
Q

Where are the polymorphisms found in MHC?

A

➝ Upper peptide binding part

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13
Q

How can different peptides bind?

A

➝ Different amino acids from different alleles means different charges and size and shape of the peptide binding groove

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14
Q

What two things do T cells recognise?

A

➝ MHC protein

➝ antigenic peptide presented by MHC

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15
Q

How does the TCR bind to MHC and why?

A

➝ with a diagonal footprint that cuts across both alpha helices with the peptide inbetween
➝ it allows it to make contact with the MHC and the peptide in the middle

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16
Q

Why are co-receptors needed when a cytotoxic T cell interacts with MHC?

A

➝ the interaction is not particularly strong

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17
Q

What acts as a co-receptor with cytotoxic T cells?

A

➝ CD8

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18
Q

What does the TCR and CD8 bind to?

A

➝ TCR binds to the alpha1 and alpha 2 domains

➝ CD8 binds to the support domains alpha 3 and beta 2M

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19
Q

What parts of the MHC is conserved and what part has polymorphisms?

A

➝ The structural part that binds to CD8 is highly conserved

➝ the part that surrounds the peptide has polymorphisms

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20
Q

Why is the structural part of the MHC highly conserved?

A

➝ the CD8 will not recognise it if it varies

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21
Q

What are 5 ways that pathogens affect MHC and give examples of which viruses use these methods?

A

➝ Inhibit MHC-I transcription - adenovirus
➝ Block TAP (HSV)
➝ Retain MHC-I in the ER (HCMV, adenovirus)
➝ Target MHC for disposal ( HCMV)
➝ Downregulate MHC-I from surface - HIV

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22
Q

What are classical NK cells?

A

➝ large granular lymphocytes that are not T or B cells

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23
Q

What marker do NK cells express?

A

➝CD56

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24
Q

How can you find NK cells under a microscope?

A

➝ they do not express TCR or CD3

25
Q

What does low NK activity correlate with?

A

➝ severe disseminating herpesvirus infections

26
Q

What does an NK deficiency lead to?

A

➝ severe viral infections early in life

27
Q

What are killer Ig-like receptors?

A

➝ Innate immune receptors that regulate the activity of NK cells

28
Q

What are leukocyte Ig-like receptors?

A

➝ Innate immune receptors that regulate the functions of NK cells

29
Q

What are KIR and LILR encoded by?

A

➝ leukocyte receptor complex

➝ on chromosome 19

30
Q

What is the function of KIR (killer Ig like receptors)?

A

➝ when KIR recognise MHC I they inhibit NK cells from releasing lytic granules

31
Q

What is a common feature of tumor cells?

A

➝ loss of MHC I

32
Q

What happens if a target cell does not express MHC I and what is this known as ?

A

➝ no KIR inhibition
➝ lytic granules will be released
➝ missing self

33
Q

Where do inhibitory KIR bind?

A

➝ the same face of MHC I as the T cell receptor

34
Q

What do inhibitory KIR recognise?

A

➝ subsets of MHC I alleles

35
Q

What are NCRs?

A

➝ Natural cytotoxicity receptors

36
Q

What is the function of NCRs?

A

➝ provide activating signals to NK cells

37
Q

What does NCR1 bind to?

A

➝ Haemagglutinin

38
Q

What does NCR2 bind to?

A

➝ binds a ligand that is expressed on tumor cells and upregulated by viral infection

39
Q

What is the ligand for NCR3?

A

➝ stress induced protein

40
Q

What does target cell death or survival depend on?

A

➝ balance of activating and inhibitory signals

41
Q

What is ADCC?

A

➝ antibody dependent cell-mediated cytotoxicity

42
Q

How does ADCC?

A

➝ Antibody binds antigens on the surface of target cells
➝ Fc receptors on NK cells recognise bound antibody
➝ Cross linking of Fc receptors signals the NK cell to kill the target cell
➝ Target cell dies by apoptosis

43
Q

Why do NK cells kill tumor cells?

A

➝ they downregulate MHC

44
Q

How do NK and T cells lyse infected cells?

A

➝ they carry granules filled with cytotoxic proteins

➝ they release the granules at the site of contact with the target cell

45
Q

What does perforin do?

A

➝ Aids in delivering contents of granules into the cytoplasm of the target cell

46
Q

What are granzymes?

A

➝ Serine proteases which activate apoptosis once in the cytoplasm of the target cell

47
Q

What is granulysin?

A

➝ Has antimicrobial actions and can induce apoptosis

48
Q

How is the CD8 apoptotic pathway triggered?

A

➝ the Fas ligand on T cells engages Fas on target cells to trigger the apoptotic pathway

49
Q

What is Fas/FasL triggered apoptosis used for?

A

➝ used to dispose of unwanted lymphocytes

50
Q

What can loss of Fas result in?

A

➝ Autoimmune lymphoproliferative syndrome ALPS

51
Q

Describe how the Fas ligand causes apoptosis?

A

➝ Trimeric Fas ligand (FasL) binds to and trimerizes Fas
➝ Clustering of death domains in the Fas cytoplasmic domains allows Fas to recruit FADD vida its death domain
➝ The clustered death effector domains of FADD recruit pro-caspase 8 via similar DEDs in the pro-caspase

52
Q

What does absence of MHC class I do to NK cells and cytotoxic T cells?

A

➝ NK : missing self - cytotoxicity

➝ Cytotoxic T : lack of recognition

53
Q

What does presence of MHC class I do to NK cells and cytotoxic T cells?

A

➝ NK : Inhibitory signal to NK

➝ Cytotoxic : TCR engagement

54
Q

What is the ligand for NK cells and cytotoxic T cells?

A 
➝ NK : class I MHC, MICA/B, immune complexes
➝ Cytotoxic : peptide-MHC class I complex
55
Q

What is the difference between cytotoxic T cell and NK receptors?

A

➝ Cytotoxic : each express a unique receptor with high specificity for a single MHC/peptide complex
➝ NK : Invariant receptor with broader specificity for MHC allele subsets

56
Q

What is the difference between how cytotoxic T cells and NK cells respond to MHC class I?

A 
➝ Cytotoxic : survey MHC class I on the surface of other cells, searching for foreign antigens 
➝ NK : respond to an absence of MHC class I
57
Q

What is the difference in activation between cytotoxic T cells and NK cells?

A

➝ Cytotoxic : Initial activation of naive T cells, followed differentiation and proliferation required
➝ NK : ready to act on encountering targets in the periphery

58
Q

What is the difference in co-receptors between cytotoxic T cells and NK cells?

A 
➝ Cytotoxic : use CD8 as a co-receptor for MHC class I 
➝ NK : do not use a co-receptors for MHC class I. and do not express CD8
59
Q

What is the difference in memory between cytotoxic T cells and NK cells?

A

➝ Cytotoxic : memory

➝ NK cells : no memory

𝓘𝓂𝓂𝓊𝓃𝑜𝓁𝑜𝑔𝓎 (14 decks)

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