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MICB 308 > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

innate immunity (2)

A
  • first line of defense in the immune response
  • non-specific
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2
Q

innate immunity: general characteristics of immunity (5)

A
  • barriers keep harmful materials from entering the body
  • direct engulfment of pathogen (phagocytosis) leads to destruction of the pathogen
  • secretion of chemokines and cytokines
  • sense the threat and type of threats using TLR receptors
  • shape the adaptive immune response
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3
Q

what kind of barriers are involved in mucosal defense (2)

A
  • chemical
  • mechanical
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4
Q

what is mucus produced by

A
  • sub-epithelial goblet cells
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5
Q

how does mucus contribute to innate immunity (2)

A
  • traps bacteria
  • contains transferrin, lactoferrin, anti-microbial peptides and lactoperoxidase
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6
Q

what are the three steps to eliminating infection in mucosal defense (3)

A
  • plasma exudation
  • immune exclusion
  • immune elimination
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7
Q

mucosal defense: plasma exudation (2)

A
  • plasma is exuded from blood vessels into the mucus site during infection
  • plasma can contain serum proteins, such as bactericidal antibodies and complement
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8
Q

mucosal defense: immune exclusion (2)

A
  • antibodies neutralize the bacteria
  • prevent binding of bacteria to host receptors for uptake
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9
Q

mucosal defense: immune elimination (2)

A
  • breach in epithelial layer results in exposure to cells of the immune system
  • elimination of bacteria by immune cells
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10
Q

what is one of the first lines of mucosal defese

A
  • nasopharynx contains mucus and cilia to prevent bacteria from entering lungs/intestines at all
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11
Q

what are some ways that the bacteria can protect itself from the host innate immune system (5)

A
  • prevent complement-mediated lysis
  • prevent phagocytosis
  • escape autophagy
  • prevent lysosomal fusion
  • prevent cytokine release
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12
Q

why did the innate immune system evolve

A
  • to recognize invariant structures in pathogens
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13
Q

what are the invariant structures we recognize on pathogens called

A
  • pathogen associated molecular patterns (PAMPs)
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14
Q

what are some examples of PAMPs (3)

A
  • carbohydrate-based (dsRNA, bacterial DNA, PG)
  • lipid-based (lipoproteins, LPS)
  • proteins (flagella)
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15
Q

what does the innate immune system use to detect pathogens (2)

A
  • pattern-recognition receptors (PRRs)
  • recognize conserved epitopes
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16
Q

what PRR recognizes the lipid A portion of LPS (a PAMP)

A
  • TLR4 and MD-2 co-receptor
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17
Q

what groups of molecules do PRRs recognize (2)

A
  • PAMPs from pathogens
  • DAMPs released from damaged cells
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18
Q

what cells are PRRs found on (5)

A
  • dendritic cells
  • macrophages
  • monocytes
  • neutrophils
  • epithelial cells
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19
Q

what occurs after innate immune recognition of pathogen (2)

A
  • direct engulfment of pathogen, leading to pathogen destruction
  • secretion of cytokines and chemokines that shape the adaptive immune response
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20
Q

TLR 4: ligand

A
  • LPS
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21
Q

TLR4 components (3)

A
  • ectodomain binds lipid A
  • transmembrane region
  • cytoplasmic region contains a toll-interleukin 1-receptor (TIR) domain
22
Q

how does TLR4/MD-2 recognize LPS (4)

A
  • LPS bind to LPS-binding protein, a free protein
  • complex interacts with CD14, a membrane receptor
  • CD14 delivers LPS to MD-2, which attaches to a TLR4
  • TLR4/MD-2/LPS complex dimerizes with another complex
23
Q

what are important domains on TLR4 for dimerization (2)

A
  • charged PO4- interface
  • neutral acyl chain interface
24
Q

TLR4/MD-2/LPS: how does signaling work after dimerization (3)

A
  • TIR domains come in close proximity
  • domains act as a scaffold to recruit adaptor proteins
  • activates two signaling pathways
25
Q

what are the two signaling pathways activated by TLR4 (2)

A
  • MyD88 pathway
  • TRIF pathway (MyD88-independent pathway)
26
Q

TLR4/LPS: what protein orchestrates signaling

A
  • the TIRAP/Mal protein
27
Q

what kind of protein is TIRAP/Mal

A
  • sorting adaptor protein
28
Q

what kind of protein is MyD88

A
  • signaling adaptor protein
29
Q

TLR4/LPS: MyD88 pathway, up to MyD88 activity (3)

A
  1. TIRAP/Mal binds to TIR domain of TLR4
  2. MyD88 binds TIRAP
  3. MyD88 associates with series of kinases
30
Q

TLR4/LPS MyD88 pathway: what occurs due to MyD88 associating with kinases (2)

A
  • activation of I kappa B kinases (IKK-1 and IKK-2)
  • results in phosphorylation of IKB
31
Q

TLR4/LPS MyD88 pathway: how is IKB normally found in the cytosol

A
  • found in complex with NFkB
32
Q

TLR4/LPS MyD88 pathway: what is NFkB

A
  • transcription factor
33
Q

TLR4/LPS MyD88 pathway: what occurs after IKB phosphorylation

A
  1. IKB is marked as degradation target for proteasomes
  2. NFkB is released and translocates to the nucleus
34
Q

TLR4/LPS MyD88 pathway: what is the result of NFkB translocation to the nucleus (3)

A
  • expression of pro-inflammatory cytokines
  • tumour necrosis factor (TNF-α), IL-12, IL-6
  • increased expression of co-stimulatory molecules
35
Q

TLR4/LPS: what is a general result of the MyD88 pathway

A
  • activation of adaptive immunity
36
Q

TLR4/LPS: when is the TRIF pathway triggered

A
  • after endocytosis of dimerized TLR4/MD-2/LPS complex into an endosome
37
Q

TLR4/LPS pathway: first half of the TRIF pathway (3)

A
  1. TRAM adaptor binds to TIR domain of TLR4
  2. TRIF binds to TRAM and leads to series of signaling events (phosphorylation events)
  3. results in activation of IRF-3 TF and translocation to the nucleus
38
Q

TLR4/LPS TRIF pathway: what is the results of IRF-3 translocation to the nucleus (3)

A
  • leads to expression of interferon-β (a type-I interferon)
  • activates expression of interferon-β inducible genes and chemokines
  • late induction of NFkB
39
Q

TLR4/LPS TRIF pathway: what is the benefit of the delayed response

A
  • ensure system isn’t overwhelmed, causing more damage
40
Q

TLR4/LPS TRIF pathway: what is the general result of this pathway

A
  • influence the adaptive immune response
41
Q

what can be the result of uncontrolled innate immune responses (3)

A
  • endothelial damage leading to multiple-organ system failure
  • acute respiratory distress syndrome (ARDS)
  • disseminated intravascular coagulation (DIC)
42
Q

what is ways that bacteria can avoid the TLR4/LPS signaling pathways (2)

A
  • innate mimicry to interfere with TLR signaling
  • lipid A modifications in LPS to affect recognition by PRRs
43
Q

TLR4/LPS: innate mimicry (2)

A
  • bacterial genomes contains genes encoding TIR-like domains
  • make TIR-containing proteins (TCPs)
44
Q

what types of bacteria practice innate mimicry against the TLR4/LPS pathway

A
  • uropathogenic E. coli (UPEC)
45
Q

monocyte model: WT bacteria vs TCP mutant

A
  • WT induced lower levels of pro-inflammatory cytokines, whereas mutants induced higher levels
46
Q

mouse model: WT bacteria vs TCP mutant

A
  • mutant was less virulent compared to the wild type
47
Q

innate mimicry: how does TCP function (3)

A
  • binds MyD88
  • reduces normal signaling in response to infection
  • reduces inflammation
48
Q

how can lipid A be modified in LPS (2)

A
  • number of acyl chains
  • charge of lipid A
49
Q

where can lipid A modifications be made in LPS (2)

A
  • modifications of acyl chains in the outer membrane
  • modifications of phosphates in the inner membrane
50
Q

endocytosis (2)

A
  • ingestion of large particles (such as bacteria)
  • uptake of fluids or macromolecules in small vesicles
51
Q

phagocytosis (2)

A
  • ingestion of large particles
  • “cell eating”
52
Q

pinocytosis (2)

A
  • uptake of fluids or macromolecules in small vesicles
  • “cell drinking”

MICB 308 (22 decks)

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