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Spring 2022 > BIOL 435 Ch. 4 Part Two (Innate Immunity) > Flashcards

BIOL 435 Ch. 4 Part Two (Innate Immunity) Flashcards

1
Q

C-type lectin receptors (CLRs)

A
  • activate innate and inflammatory responses

- generally recognize CHO componenents of fungi, viruses, mycobacteria, parasites and allergens

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2
Q

CLRs trigger pathways

A 
-leading to TFs that induce expression of proinflammatory cytokines
>INF alpha/beta
>IL-1beta
>TNF
>IL-23
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3
Q

NOD-like receptors

A
  • nucleotide oligomerization domains-receptors
  • cytosolic PRRs activated by intracellular PAMPs and DAMPs
  • induce expression of genes encoding antimicrobial proteins and peptides
  • initate autophagy
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4
Q

initiate autophagy (NOD-receptors)

A

-by forming autophagosomes that fuse with lysosomes to then kill bacteria

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5
Q

NOD1 and NOD2

A
  • bind PAMPs of intracellular microbial components

ex. bacterial cell wall fragments

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6
Q

RIG-1-like receptors (RLRs)

A
  • recognize viral dsRNAs
  • function as cytosolic PRRs
  • trigger signalling pathways that activate IRFs and NF-kappa beta TFs
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7
Q

IRFs

A
  • interferon regulatory factors
  • lead to increased expression of interferons (IFN-alpha and IFN-beta)
  • potent antiviral cytokines
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8
Q

dsRNA

A

-only with viruses

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9
Q

PRR signalling pathways

A 
-activate expression of a large variety of genes
>antimicrobial peptides
>type 1 interferons
>cytokines
>chemokines
>enzymes (iNOS an COX2)
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10
Q

COX2

A
  1. Arachidonate to prostaglandins: pain sensations

2. Promote inflammation

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11
Q

Type 1 interferons

A
  • IFN-alpha and IFN-beta
  • potent antiviral effects
  • inhibit viral replication, transcription and translation
  • activate NK cells
  • regulate macrophages and T-cells
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12
Q

signalling through TNF receptors

A
  • binding of TNF activates cytoplasmic death domain (DD)
  • response depends on cell and its environment
    1. Cell survival and immune response
    2. Apoptosis: cut in a clean way (doesn’t lead to inflammation)
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13
Q

innate immune response steps

A
  1. Leukocytes in blood respond to chemical attractants released by pathogens and signals from nearby injuried cells
  2. Leukocytes squeeze between cells of the capillary wall
  3. Within damaged tissue, neutrophils release chemicals to break apart pathogens
    >monocytes differentiate into macrophages
    >phagocytosis
    >take some bacteria to a lymph cell to start an adaptive response
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14
Q

phagocytosis

A

-engulfment and internalization of materials for their clearance and destruction
-microbes are recognized by receptors on phagocytes
>may recognize soluble opsonin protein bound to microbes

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15
Q

phagocytes

A
  • macrophages, neutrophils, dendritic cells
  • may recognize PAMPs directly through PRR binding
  • may be induced indirectly through opsonization
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16
Q

opsonins

A
  • soluble pattern recognition proteins
  • mannose binding lectin (MBL)
  • complement proteins
  • C-reactive protein
  • Antibodies
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17
Q

opsonization

A
  • ‘to make tasty’

- the process of chemical modification that enhance binding to a phagocytoic cell=enhances phagocytosis

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18
Q

phagosomes

A

-fuse with lysosomes or granules

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19
Q

destruction occurs through

A
  • enzyme degradation
  • antimicrobial proteins
  • toxic effects of ROS and RNS
20
Q

respiratory burst

A

-intracellular killing
-bleach fireball
-ROS lead to cell death
>neutrophils sometimes commit suicide for the greater good

21
Q

cell death induced by receptor activated signal pathways

A
  • apoptosis
  • NETs
  • pyroptosis
22
Q

apoptosis

A
  • cell death induced by TNF binding to TNFR, NK cells and T cytotoxic cells
  • clean, tidy, controlled
23
Q

NETs

A
  • neutrophil extracellular traps

- activation requires NADPH oxidase and generation of ROS

24
Q

pyroptosis

A
  • induced by inflammasome activation eliminates infected macrophages allowing release of IL-1beta and IL-18
  • messy
25
Q

IL-1beta and IL-18

A
  • made in cytosol, not in a vesicle
  • need to be cleaved to be activated
  • then cells commit suicide to release them
26
Q

apoptosis steps

A
  1. Cell shrinks, chromatin condenses
  2. Membrane starts blebbing, organelles disintegrate
  3. Nucleus and organelles collapse, membrane continues to bleb
  4. Apoptotic bodies form
  5. Macrophages phagocytose apoptotic bodies
    * no inflammation
27
Q

NETs steps

A
  1. Signals from PRR activate neutrophils
  2. Phagosome NADPH oxidase (PHOX) is induced and intracellular membrane begin to break down
  3. Granule enzymes neutrophils elastase (NE) and myeloperoxidase (MPPO) enter the nucleus and modify histones
    >chromatin decondenses
  4. PM ruptures and cytoplasm and nucleoplasm are expelled forming NETs
  5. Cells die form NEToses
28
Q

inflammasome formation

A
  • may be due to signalling of TLR, NOD-like receptor and others
  • allows cleavage of procaspase 1 to caspase-1
29
Q

caspase-1

A

-cleaves pro-IL-1beta and pro-IL-18 into IL-1beta and IIL-18

>may lead to cell death to release them (pyropotosis)

30
Q

IL-1beta

A

-potent inflammatory cytokine (and IL-18)

31
Q

proinflammatory cytokines and chemokines triggered by

A

-innate responses to infection, damage or harmful substances

32
Q

early components of inflammation include

A
  • increase vascular permeability

- recuritment of neutrophils and other leukocytes from the blood to the side of damage/infection

33
Q

5 inflammatory signs

A
  1. Heat: vasodilation, increased blood flow
  2. Redness: increased blood flow
  3. Swelling: plasma through gaps
  4. Pain: pressure on nocireceptors
  5. Loss of function
34
Q

inflammatory response steps

A
  1. Tissue damage
    - release chemoattracts and vasoactive factors
    - these trigger a local increase in blood flow and capillary permeability
  2. Influx of fluid and cells
  3. Neutrophils and other phagocytes migrate to site of inflammation
  4. Phagocytes and antibacterial substances destroy bacteria
35
Q

later stages of inflammation

A
  • acute phase responses (APRs)
  • induced by acute inflammaoty triad
  • incrased synthesis/secretion of antimicrobial proteins by liver
36
Q

antimicrobial liver proteins examples

A
  • MBL: mannose binding lectin
  • CRP: C-reactive protein
  • complement components
  • activate other processes that help eliminate pathogens
37
Q

acute inflammatory triad

A
  1. IL-1
  2. TNF-alpha
  3. IL-6
38
Q

innate lymphoid cells (ILC)

A
  • derived from common lymphoid progenitor cells

- include NK cells and 6 other ILC populations

39
Q

NK cells found in

A

-lymphoid tissue and recirculate

40
Q

other ILC found

A

-in epithelium

41
Q

ILC group based on

A

-cytokines produced

42
Q

ILCs lack PRRs

A

-are not activated directly by pathogens

43
Q

NK cells

A
  • lymphocytes with innate immune functions
  • express a limited set of receptors for self-proteins
  • activated and perform 1 of 2 functions
44
Q

NK receptors induced by

A
  • infections
  • malignant transformations (ex. cancer)
  • other stresses
45
Q

activated NK cell functions

A
  1. Kill altered self-cell by releaseing perforin and gronzymes inducing apoptosis
  2. Produce cytokines that induce adaptive responses against the altered self-cell

Spring 2022 (54 decks)

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