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PABI 6100 Immunobiology > 2. Innate Immunity > Flashcards

2. Innate Immunity Flashcards

1
Q

What are the 3 lines of defence in innate immunity?

A
  1. Physical/ Chemical barriers
    > epithelial layers of skin/ mucosal tissue/ glandular tissue
    > acidic pH/ antimicrobial proteins
  2. Cellular responses
    > innate immune cells recognize pathogens and trigger phagocytosis/ production of antimicrobial proteins/ cytokines
  3. Activation of adaptive immune responses
    > through cytokines/ DCs that present antigens
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2
Q

What are the main phagocytic cells?

A
  • macrophages/ neutrophils/ DCs in tissues
  • monocytes in blood
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3
Q

What are the 5 steps of phagocytosis?

A
  1. Pathogen binds to PRR on pseudopodia
  2. Pathogen ingested forming a phagosome
  3. Phagosome fuses with lysosome
  4. Pathogen is killed/ digested by low pH of lysosomal enzymes
  5. Digestion products are released from cell
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4
Q

How are phagocytosed microbes killed?

A
  • antimicrobial proteins/ peptides
    > defensins- disrupt membranes of pathogens
  • acid-activated hydrolytic enzymes
    > lysozymes- disrupt bacterial cell wall
  • molecules that mediate oxidative attack
    > ROS/ RNS- damage intracellular components
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5
Q

How do antimicrobial ROS/ RNS alter microbes?

A
  • oxidation/ hydroxylation/ chlorination/ nitration
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6
Q

How do phagocytes recognize microbes?

A
  • Direct recognition > through PRRs
  • Indirect recognition > through opsonin receptors
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7
Q

How do phagocytes respond to microbes?

A
  • killing through phagocytosis/ complement activation
  • inflammation (cytokines)
  • initiation of adaptive responses
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8
Q

What is direct recognition by phagocytes?

A
  • PRRs on phagocytes bind to PAMPs on surface of microbes
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9
Q

What are some examples of PRRs/ PAMPs?

A
  • PRRs > mannose receptors/ SR-A
  • PAMPs > mannans/ LPS (lipopolysaccharide)
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10
Q

What are MAMPs?

A
  • PAMPs can be expressed by microbes whether or not pathogenic
  • MAMPS > more general term can be used
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11
Q

What is indirect recognition by phagocytes?

A
  • opsonin receptors on phagocytes bind to opsonins
  • opsonins > soluble proteins that bind to PAMPs on surface of microbes
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12
Q

What are some examples of opsonin receptors/ their ligands (opsonins)?

A
  • opsonin receptors > CD91/ FcyRs
  • opsonins > L-ficolin/ C-reactive protein
  • PAMPS > acetylated sugars/ phosphorylcholine
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13
Q

What is opsonization?

A
  • phagocyte recognition of opsonins bound to microbial PAMPs enhances phagocytosis
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14
Q

How does phagocytosis contribute to cell turnover/ clearance of dead cells?

A
  • PPRs on phagocytes recognize DAMPs on dead/ dying/damaged cells
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15
Q

How does RBC cell turnover occur?

A
  • as RBCs age, phosphatidyl serine flips from inner > outer membrane leaflet
  • phosphatidyl serine is recognized by its receptor on macrophages
    > phagocytosis/ degradation of old RBCs
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16
Q

What are the 4 families of PRRs?

A
  • TLRs > toll-like receptors
  • CLRs > c-type lectin receptors
  • RLRs > retinoic acid-inducible gene-I-like receptors
  • NLRs > nod-like receptors
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17
Q

Where are TLRs located/ what do they do?

A
  • exist both on PM/ lysosome and endosome membranes
  • TLRs on plasma membrane > recognize PAMPs on outer surface of extracellular microbes
  • TLRs on endosomes/ lysosomes > recognize internal microbial components
  • detect DAMPS from dead/ dying/damaged tissues
  • do not promote phagocytosis
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18
Q

Where are CLRs located/ what do they do?

A
  • plasma membrane receptors
  • recognize carbohydrate components of extracellular pathogens
19
Q

Where are RLRs located/ what do they do?

A
  • soluble PRRs that reside in cytosol
  • sense viral infection > distinguish viral/ cellular RNA
  • bind viral RNA in cytosol of infected cells
20
Q

Where are NLRs located/ what do they do?

A
  • cytosolic proteins activated by intracellular PAMPs/ DAMPs
  • some activate gene transcription > cytokines/ antimicrobial proteins
  • some assemble with other proteins into a complex > activates proteases that convert IL-1 precursor > mature form
    > IL-1 is very inflammatory > NLR complex = Inflammasome
21
Q

What are inflammasomes?

A
  • complexes of NLRs that activate proteases > convert IL-1 precursor > inflammatory mature form of IL-1
22
Q

How does PRR signalling contribute to the expression of innate immunity proteins?

A
  • PRR-activated signalling pathways > expression of genes with functions in immunity > production of antimicrobial proteins/ cytokines/ chemokines
23
Q

What is the structure of TLRs?

A
  • exterior domain
    > leucine-rich repeats (LRRs) make up the ligand-binding domain
  • membrane-spanning domain
  • TIR domain (intracellular)
    > interacts with other members of TLR signaling pathway
24
Q

What happens when TLRs bind their ligands?

A
  • induced to dimerize
25
Q

What is the cellular location of TLRs?

A
  • TLRs that bind extracellular ligands > in plasma membrane
  • TLRs that bind internal microbial components > lysosomes/ endosomes
  • upon ligand binding, the TLR4/4 dimer moves from plasma membrane > endosomal/ lysosomal compartment
26
Q

How is TLR signalling initiated?

A
  • TLR-signalling is initiated after ligand-induced TLR dimerization
  • the signal transduction pathway activated by TLR dimer is determined by the protein adaptor that binds to TLRs cytoplasmic TIR domain
    > 2 key adaptors recruited to TLR dimers: MyD88 (most)/ TRIF
27
Q

What are the steps in TLR signalling? (signal transduction pathway)

A
  • MyD88 adaptor protein binds to cytoplasmic TIR domain of TLRs
    > recruits kinases IRAK1/ IRAK4 > phosphorylate self/ other proteins
28
Q

What are 4 common strategies used in many signalling pathways?

A
  • ligand binds to receptor > conformational change in receptor ex) dimerization of TLRs
  • some receptors require receptor-associated molecules
    > if cytoplasmic tails too short, can not get phosphorylated
  • tyrosine kinases activated > tyrosine phosphorylation
  • ubiquitination > may inhibit/ enhance signal transduction
29
Q

What do adaptor proteins do?

A
  • gather members of signalling pathways
30
Q

What is the complement system?

A
  • set of serum proteins that cooperate with immune system to eliminate pathogens
31
Q

How does the complement system cooperate with the immune system to eliminate pathogens? (3x)

A
  • various complement components bind/ opsonize pathogens
  • some complement proteins elicit inflammatory responses/ clear immune cells/ eliminate apoptotic cells
  • MAC assembled from complement proteins > kills pathogens by creating pores in microbial membranes
32
Q

What are the 7 functional categories of complement components?

A
  • complement pathways initiated by proteins that bind to pathogens
    > C1q = initiator of cascade
  • enzymes are the central proteins of the complement cascade
    > C3/ C5 convertase (cleave C3/C5 > releasing active components)
  • opsonization (C3b opsonin)
  • inflammation (C5a anaphylatoxin)
  • generation of MAC
  • complement effectors act by binding to their receptors (CR1/CR3)
  • regulatory proteins limit the effects of complement by promoting their degradation/ preventing their binding to host cells
33
Q

What is psoriasin?

A
  • antimicrobial protein secreted by skin that kills E.coli
34
Q

Why does lysozyme not damage human cells?
> antimicrobial protein that cleaves glycosidic bonds in cell walls of bacteria

A
  • mechanism of action > cleaves glycosidic bonds in cell walls
    > human cells do not have cell walls
35
Q

What are the 5 hallmarks of inflammation?
(localized inflammatory response)

A
  • redness/ swelling/ heat/ pain/ loss of function
36
Q

What are the 3 steps of inflammation?
(innate response triggered by local infection/ tissue damage)

A
  • Initiation > activation of macrophages/ DCs by PAMPS/ DAMPs
    > release of mediators IL-1/ histamine > vasodilation
    > recruitment of neutrophils/ monocytes
  • Amplification > recruited cells do phagocytosis/ release additional mediators
  • Resolution > cytokines (mainly TNF/ IL-1/ IL-6) induce AFR
    > cytokines act on hepatocytes > secrete AFR proteins at ↑ levels
37
Q

What are AFR proteins?

A
  • serve as opsonins/ activate complement-mediated attack on microbe
  • ex) mannose-binding lectin/ C-reactive protein
38
Q

What is NETosis?

A
  • form of regulated cell death induced by PAMP-activated PRR signalling
  • catching/ killing pathogens by neutrophil extracellular traps (NETs)
    > NETs are filaments of chromatin that neutrophils expel to entrap pathogens
39
Q

What are the steps of NETosis?

A
  • signals from PRRs activate neutrophils
  • NADPH oxidase activated > generation of ROS damages cell compartments
  • cell membrane disintegrates > cellular contents (chromatin filaments) expelled to form NETs
  • NETs trap pathogens > cell dies from NETosis
40
Q

How do NETs indirectly contribute to innate immunity?

A
  • DNA/ chromatin components serve as DAMPs
    > further activates innate responses
41
Q

What are the innate immune response mechanisms of plants?
- no phagocytosis

A
  • generation of ROS/ RNS
  • ↑ internal pH
  • induction of antimicrobial peptides (including defensins)
  • induction of antimicrobial enzymes > digest cell walls
  • production of organic molecules > antibiotic activity (phytoalexins)
  • plants have PRRs with leucine-rich repeats > recognize PAMPs
42
Q

What are some structural changes of plants in response to pathogens?

A
  • binding to PRRs induces closure of leaf stomata
    > limits infection by preventing any further microbial invasion
  • strengthening walls of surrounding noninfected cells
  • induced death (necrosis) of cells surrounding infection to limit spread
43
Q

What is the only vertebrate that does not make antibodies?

A
  • Jawless fish > have VLRs instead (variable lymphocyte receptors)
44
Q

How do immune responses differ between multicellular organisms?
> plants/ invertebrate animals/ vertebrate animals

A
  • plants > only innate immunity/ no phagocytosis
  • invertebrates > innate immunity/ phagocytosis
  • vertebrates > both innate/ adaptive immunity

PABI 6100 Immunobiology (6 decks)

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