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lolmyi > L23: NK Cells > Flashcards

L23: NK Cells Flashcards

1
Q

What are the progenitors of NK cells?

A

→common lymphoid progenitor

→same as Tcells and Bcells

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2
Q

What do cytotoxic cells destroy?

A

→Cells infected with bacteria, viruses or parasites

→Tumour cells

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3
Q

What is CTL killing controlled by?

A

→T cell receptor recognition, with CD8 acting as a co-receptor

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4
Q

Compare the specificity of NK cells and CTLs

A

→CTL are highly specific

→NK cells have broad specificity

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5
Q

Why do we need more than one type of cytotoxic lymphocyte?

A

→To combat infection in the period before a T cell response develops

→To provide an alternative system when a tumour or infected cells evade Cytotoxic T cell responses

→To provide an additional mechanism for killing infected targets via antibody recognition

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6
Q

How long after first encounter do CTL kick in?

A

→7 days

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7
Q

What is the link between NK cells and cancer?

A

→Medium and high cytolytic function was associated with reduced cancer risk

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8
Q

Summarise intracellular proteins presentation on MHC1

A

→antigen processed in phagosome
→peptide transport into ER
→peptide binding by MHC1
→MHC1 presents peptide of cell surface

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9
Q

Describe the structure of MHC1

A

→2 alphas helices forming edges of groove.

→Beta sheets forming base of peptide binding groove

→B2 macroglobulin supports peptide binding groove

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10
Q

Compare alpha helices and beta2- microglobulin

A

alpha helices
→polymorphic
→glycosylated
→inserted in membrane

beta2-microglobulin
→not polymorphic
→not glycosylated
→not inserted in membrane

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11
Q

Which chromosome is the MHC gene found?

A

→chromosome 6

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12
Q

How many MHC1 and MHC2 proteins?

A

→3 MHC1(6 MHC1 genes because of two alleles)

→3 MHC2

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13
Q

What is the most genetically diverse genes?

A

→HLA

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14
Q

Where is the polymorphs found in MHC?

A

→in the upper peptide-binding part

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15
Q

Where is variation found in the MHC1 and MHC2 binding groove?

A

→MHC1 in the pocket of groove

MHC2 in the beta chain groove

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16
Q

What are pockets in the MHC groove formed from?

A

→amino acids

→creates different charges

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17
Q

How long is the peptide that binds into pockets?

A

→9 amino acids in length and they will bind to corresponding pockets

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18
Q

What two things do TCR recognise?

A

→MHC protein itself

→Antigenic peptide presented by MHC protein

19
Q

In what two situations would someone have foreign MHC1?

A

→pregnancy

→transplant

20
Q

How does TCR bind to MHC1?

A

→diagonal footprint that cuts across both alpha helices of MHC1 with the peptide in between

21
Q

What is a co-receptor for MHC1?

A

→CD8

→CD8 binds to the support domains (a3 and b2m)

22
Q

Which domains does TCR bind to on MHC1?

A

→a1a2 domains

23
Q

How do pathogens subvert presentation by MHC-I?

A

→Inhibit MHC-I transcription (adenovirus)

→Block peptide transport into the endoplasmic reticulum (HSV)

→Retain MHC-I in endoplasmic reticulum (adenovirus, HCMV)

→Target MHC-I for disposal from the endoplasmic reticulum (HCMV)

→Downregulate MHC-I from cell surface (HIV)

24
Q

What is the normal function of KIR in healthy cells?

A

→KIR recognise MHC-I they inhibit NK cells from releasing lytic granules

25
Q

What does KIR cells do when there is no MHC?

A

→no KIR inhibition,
→lytic granules will be released to lyse the target
→missing self

26
Q

Where does KIR bind on MHC1?

A

→to the same face of MHC-I as the T cell receptor

→binds just one end of the MHC but sees the top and bottom of grove and the antigen- sees a lot less than TCR

27
Q

Compare the specificity of KIR and TCR?

A

→KIR has less specificity than TCR
→KIR can recognise subsets of MHC1
→KIR is also polymorphic

28
Q

What other natural cytotoxicity receptors are found on NK cells and what do they bind to?

A

→NKp46 is known to bind viral hemagglutinin

→NKp44 – binds a ligand that is expressed on tumor cells and upregulated by viral infection

→Ligand for NKp30 is a stress induced
protein

29
Q

What does target cell death depend on?

A

→depends on balance of activating and inhibitory signals

30
Q

Why do NK cells kill tumour cells?

A 
→downregulating the expression of MHC class I
→tumour cells also induce stress signals that activate NK cells
31
Q

Describe ADCC

A

→Antibody-dependent cell-mediated cytotoxicity

→At the point of budding, viral proteins are expressed and antibodies are bound

→NK cells express a receptor that recognizes the Fc portion of antibodies

→ receptor delivers a strong activating signal when it recognizes antibodies bound to a cell surface

→Results in lysis of the target cell

32
Q

Describe the lysis mechanism of NK cells

A

→NK cells and T cells carry granules filled with cytotoxic proteins

→Release cytotoxic granules at site of contact with target cell

33
Q

What are three proteins in granules for lysis?

A

→perforin
→granzymes
→granulysin

34
Q

What is the function of perforin?

A

→aids in delivering granules into cytoplasm of target cells

35
Q

What is the function of granzymes?

A

→serine proteases

→activates apoptosis once in cytoplasm

36
Q

What is the function of granulysin?

A

→has antimicrobial actions

→can help induce apoptosis

37
Q

Describe the immunological synapse

A

→T cell receptors and co-receptors cluster at the site of cell-cell contact
→Triggers reorganisation of cytoskeleton
→polarises the T cell to release effector molecules at the point of contact

38
Q

Why is polarisation of TCRs and co-receptors important?

A

→to prevent killing of healthy nearby cells

39
Q

How does CD8 trigger apoptosis of Fas/FasL interaction?

A

→Fas ligand (FasL) on T cells engages Fas on target cells to trigger apoptotic pathway

40
Q

Why is FasL apoptosis used?

A

→used to dispose of unwanted lymphocytes

41
Q

What does loss of FAD result in?

A

→autoimmune lymphoproliferative syndrome (ALPS)

42
Q

Compare NKs and CTLs

A

→CTLs use CD8 as a co-receptor for MHC class I

→NK do not use a co-receptor for MHC class I, do not express CD8

43
Q

Describe the FasL/Fas apoptosis pathway

A

→trimeric Fas ligand binds and trimerizes Fas
→Clustering of Death Domain in Fas cytoplasmic domains allow Fas to recruit FADD via death domain
→Clustered death effector domains of FADD recruit procaspase 8 via similar DED in the pro-caspase

lolmyi (31 decks)

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