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MDSC 321 > Lecture 9: Innate Pathogen Recognition > Flashcards

Lecture 9: Innate Pathogen Recognition Flashcards

1
Q

Does the innate immune system recognize specific cells?

A

No, just self and non-self

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2
Q

What does the innate immune system recognize

A

Molecular patterns on different pathogens but absent from self

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3
Q

What does PAMP stand for?

A

pathogen associated molecular patterns

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4
Q

What are PAMPS recognized by?

A

Various pattern-recognition receptors (PRRs)

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5
Q

Where are PRRs located?

A

On most effector cells

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6
Q

Where does each PRR belong?

A

Cell surface and cytoplasmic receptors

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7
Q

What are the four classes of receptors reviewed?

A
  • TOLL-like receptors
  • Nucleotide binding domain leucine rich repeat receptors
  • Formylated-peptide receptors
  • retinoic acid inducible gene like
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8
Q

What is the abbreviation for TOLL-like receptors?

A

TLRs

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9
Q

What is the abbreviation for Nucleotide-binding domain leucine-rich repeat receptors

A

NLRs, NOD-like receptors

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10
Q

What is the abbreviation for Formylated-peptide receptors

A

FPRs

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11
Q

What is the abbreviation for retinoid-acid inducible gene-like

A

RLRs

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12
Q

Where were TLRs initially discovered?

A

In the fruit fly

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13
Q

What was TOLL initially thought to only do then found to do both in the fruit fly?

A
  • Initially played a role in patterning
  • then the translation and synthesis of antimicrobial peptides
  • defence against gram-positive bacteria and fungal pathogens
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14
Q

How many expressed TLR genes are in humans?

A

10

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15
Q

What is a ligand?

A

A signalling molecule

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16
Q

What are TLRs made of in there extracellular region (outside of the cell)?

A

Around 20 leucine-rich repeat

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17
Q

What are leucine-rich repeat?

A

Proteins that make a half circle (Horse shoe) shape

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18
Q

1A. Explain how bacteria activate TLRs in flies?

A

Recognition of bacteria by pathogen recognition receptors results in a bunch of steps that lead to a proteolytic (breakdown) splitting of a dimer of spatzle

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19
Q

2A. Explain how spatzle induces dimerization?

A

The split spatzle binds 2 TOLL molecules inducing dimerization

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20
Q

3A. What is dimerized TOLL able to do?

A

recruits:

  • 2 dMyD88
  • 2 Pelle
  • 1 TRAF3
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21
Q

4A. What does TRAF3 do?

A

Binds cactus kinase (enzyme) which introduces a phosphate group into cactus

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22
Q

5A. What does phosphorylated cactus do?

A

Releases transcription factor DIF

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23
Q

6A. What does DIF do?

A

Transcription and synthesis of antimicrobial peptides

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24
Q

Does each TLR have a different ligand specificity?

A

yes

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25
Q

What are mammalian TLRs dependent on?

A

dimerization

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26
Q

What do mammalian TLRs bind directly to?

A

pathogen associated molecular patterns

27
Q

What happens when PAMPs bind to TLRs

A

It induces dimerization of the TLR

28
Q

What does the dimerization of TLRs (mammals) do?

A

It brings the cytoplasmic tails of the TLR molecules into close proximity

29
Q

What does the tails of the TLRs in close proximity do?

A

Induces binding of signalling adapter molecules

30
Q

What is the signalling adapter molecule for all TLRs except TLR-3?

31
Q

What is the signalling adapter molecule for TLR-4,3

32
Q

1B. What does the binding of MyD88 do?

A
  • binding of MyD88 and MAL to TLR

- allows for binding of IRAK to MyD88

33
Q

2B. What does the binding of IRAK to MyD88 do?

A
  • IRAK binds TRAF-6 & TRICA1

- these provide foundation for activation of TAK1

34
Q

3B. What does the activation of TAK 1 do?

A

TAK1 phosphorylates IKK

35
Q

4B. What does IKK do?

A

IKK phosphorylates IkB

36
Q

5B. What does IkB do?

A

IkB is degraded releasing NFkB

37
Q

6B. What does NFkB do?

A
  • NFkB translocates to the nucleus

- transcribes target genes

38
Q

1C. What does the binding of TRIF allow for?

A
  • binding of TRIF to TLR3 or 4

- allows for the binding of the kinases TBK1 and IkKe

39
Q

2C. What do the kinases do?

A
  • kinases become phosphorylated

- resulting in their activation

40
Q

3C. What do the activated kinases do?

A

-activated kinase phosphorylates IRF3

41
Q

4C. What does IRF3 do?

A

-IRF3 translocates to the nucleus and transcribes target genes

42
Q

Do we generate different cell responses based on the PAMP?

43
Q

Since most TLRs use the same signalling adapter molecule MyD88 how do we generate different cellular responses?

A

This is possible because:

  • subcellular location of the molecule
  • signal duration
  • additional signalling molecules
44
Q

What is subcellular location

A

The location of TLRs are different not all are transmembrane receptors some are located in the endosome

45
Q

What does the TLRs in the endosome recognize?

A

PAMPs from within the pathogen, RNA and DNA

46
Q

What is signal duration?

A

The duration of the TLR signal can vary based on:

  • magnitude of the signal
  • number of receptors involved
  • negative regulators of the TLR
47
Q

What does signal duration modify?

A

Resulting gene transcription profile

48
Q

What does subcellular location modify?

A

Which target genes are transcribed

49
Q

What is additional signalling molecules (specificity)

A

Most use MyD88 some use TRIF or a combination of TRIF and MyD88

50
Q

Is TRIF regulated negatively by Tollip?

51
Q

What do the different signalling molecule combinations result in?

A

Different cellular responses

52
Q

What are NOD-like receptors (NLRs)?

A

NLRs are cytoplasmic receptors

53
Q

What differs between NLR groups?

A

They differ depending on their amino-terminal structural motifs (distinct pattern on DNA or protein)

54
Q

What does NOD have

A

N-terminal CARD motif

55
Q

What does NLRP have?

A

N-terminal pyrin domain

56
Q

1D. What is the first step in NOD-like receptors?

A
  • binding PAMPs to NOD1 or 2

- results in dimerization of the NOD

57
Q

2D. What happens in NOD after dimerization?

A

-dimerization facilitates recruitment of the kinase RIPK2 to the CARD domain of the NOD

58
Q

3D. What happens after RIPK2 is recruited to the CARD domain of NOD?

A

-RIPK2 phosphorylates TAK1, activating it

59
Q

4D. What happens in NOD-like receptor after TAK1 is activated?

A

Follows same steps as 3B-6B, binding of MyD88

60
Q

What is the formylated peptide receptor (FPRs)?

A
  • Transmembrane pattern recognition receptor

- G-protein coupled receptor family

61
Q

Where are formylated peptide receptors mainly expressed?

A

Neutrophils

62
Q

What do formylated peptide receptors recognize?

A

Bacterial formylated peptides

63
Q

What does activation of formylated peptide receptors give rise to?

A

Important secondary messengers:

  • Ca2+
  • IP3
  • cyclic AMP
64
Q

What do formylated peptide receptors lead to?

A

-activation
-polarization
-mobility
in neutrophils

MDSC 321 (21 decks)

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