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BSCI 2150 > Week 13.1 Innate Immunity > Flashcards

Week 13.1 Innate Immunity Flashcards

1
Q

Primary defenses

A

-physical and chemical barriers:
-ciliated epithelium
-alveolar macrophages
-acid
-bile
-urine flow
-normal flora
-body temperature
-skin
-tears
-mucous

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2
Q

Antimicrobial secretions

A

-toxic to pathogens
-defensins, bactericidal/permeability increasing peptides
-lysozyme
-lactoperoxidase

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3
Q

Defensins

A

short peptides w/ broad antimicrobial activity (cell wall and membrane disruption) and/or immune signaling

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4
Q

Bactericidal/permeability increasing peptides (BPIs)

A

short peptides w/ broad antimicrobial activity and/or immune signaling

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5
Q

Lysozyme

A

breaks down peptidoglycan cell wall

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6
Q

Lactoperoxidase

A

generates reactive oxygen species

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7
Q

Metal ion-binding proteins sequester…

A

iron, zinc, or magnesium

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8
Q

Iron

A
  1. Why pathogens need it: TCA Cycle, electron transport, oxidative phosphorylation, aromatic biosynthesis, peroxidase, & superoxide dismutase
  2. Sequestered by: lactoferrin, ferritin, transferrin
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9
Q

Zinc

A
  1. Why pathogens need it: RNA polymerase, DNA polymerase, & alkaline phosphatase
  2. Sequestered by: calprotectin & metallothioneins
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10
Q

Magnesium

A
  1. Why pathogens need it: Superoxide dismutase
  2. Sequestered by: calprotectin
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11
Q

Internal cellular defenses (innate immunity)

A

monocytes
macrophages
neutrophils
NK cells
mast cells
dendritic cells
eosinophils
basophils

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12
Q

Monocytes

A

differentiates into macrophages and dendritic cells in response to inflammation

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13
Q

Macrophages

A

engulfs and kills pathogens and cancerous cells; stimulates other immune cells

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14
Q

Neutrophils

A

engulfs and kills pathogens

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15
Q

Natural Killer (NK) cells

A

kills tumor cells and virus infected cells

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16
Q

Mast cells

A

releases histamine, inflammatory response

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17
Q

Dendritic cells

A

triggers adaptive immunity (T cells)

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18
Q

Eosinophils

A

production of toxic molecules to kill pathogens and regulation of inflammation

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19
Q

Basophils

A

production of toxic molecules to kill pathogens and regulation of inflammation

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20
Q

Innate cellular response steps

A
  1. Detection of an infection (PAMPs and PRRs)
  2. Chemical signaling (cytokines, chemokines, pyrogens, interferons)
  3. Destruction of pathogens and damaged/infected cells
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21
Q

What cells detect pathogens w/ PRRs?

A

epithelial cells and leukocytes

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22
Q

Types of pathogen recognition receptors

A
  1. Toll-like receptors
  2. NOD-like receptors
  3. RIG-1-like helicases and MDA-5L
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23
Q

Toll-like receptors

A

transmembrane proteins that recognize molecules shared broadly by pathogens (broad spectrum)

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24
Q

NOD-like receptors

A

intracellular proteins that help regulate the immune response by releasing cytokines, chemokines, or apoptosis

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25
Q

RIG-1-like helicases and MDA-5L

A

intracellular proteins that detect ssRNA viruses and help regulate the immune response

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26
Q

What are PRRs activated by?

A

pathogen associated molecular patterns (PAMPs)

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27
Q

What are PAMPs?

A

molecules that are characteristic of pathogens and are not normally found inside the body

28
Q

Examples of PAMPs

A

Lipopolysaccharides (LPS)
Lipoprotein
Peptidoglycan
Lipoteichoic acids
RNA/DNA
Flagella
Membranes

29
Q

What can PRRs also recognize besides PAMPs?

A

damage associated molecular patterns (DAMPs)

30
Q

What are DAMPs?

A

host signaling molecules that are produced by dying or damaged cells (regardless of infection) to activate the innate immune response

31
Q

Cell signaling

A

When a PAMP is detected by a PRR, chemical signals (cytokines and chemokines) are secreted to tell the body an infection is starting

32
Q

Cytokines

A

secreted molecules that cause an effect in another cell ex: interleukins, interferons, or growth factors

33
Q

Chemokines

A

a class of cytokines that attract white blood cells (leukocytes)
ex: histamine

34
Q

Proinflammatory cytokines stimulate what kind of response?

A

an acute inflammatory response

35
Q

Acute inflammatory response

A

-capillary widening > increased blood flow > heat
-increased permeability > fluid release into tissues > redness and swelling
-attraction of leukocytes > extravasation of leukocytes to site of injury > tenderness
-systemic response > fever and proliferation of leukocytes > pain

36
Q

Objectives of inflammation

A

-DESTROY the pathogen and REMOVE its by-products from the body
-CONFINE the pathogen and its products to limit the damage
-REPAIR OR REPLACE damaged tissue

37
Q

What are the first cytokine signals that both stimulate an acute inflammatory response?

A

IL-1 and TNF-alpha (tumor necrosis factor)

38
Q

IL-1

A

-induced by PAMPs
-produced by macrophages, endothelial cells, and epithelial cells
-promotes inflammation

39
Q

TNF-alpha

A

-induced by PAMP
-produced by macrophages and T cells
-promotes inflammation, vascular permeability, chemotaxis, and apoptosis

40
Q

TNF-alpha promotes inflammation

A

-Activates mast cells to release histamine, which causes vasodilation
-Induces fever in the hypothalamus
-Enhances production of proinflammatory cytokines (IL-1 and IL-6)

41
Q

TNF-alpha helps recruit immune cells

A

-Stimulates endothelial cells to express adhesin molecules
-Stimulates the production of chemokines to attract leukocytes
-Loosens epithelial tight junctions to allow diapedesis
-Activates neutrophils and macrophages

42
Q

How are neutrophils and macrophages recruited to infected tissue?

A

By chemokines that attract white blood cells; they squeeze through blood vessels aided by adhesin molecules and gaps promoted by histamine and TNF-alpha

43
Q

Destruction of pathogens and damaged/infected cells

A

phagocytosis

44
Q

Phagocytosis

A

ingestion of bacteria or other material by a phagocyte, stimulates the macrophage to produce more proinflammatory cytokines

45
Q

Phagocytosis steps

A
  1. Attachment
  2. Ingestion
  3. Digestion
46
Q

Phagocytosis Attachment step

A

Detect and attach to pathogens using specialized receptors

47
Q

Phagocytosis Ingestion step

A

Engulfs pathogen by surrounding it with the phagocytes membrane
-results in membrane-bound pathogen inside the cell aka phagosome

48
Q

Digestion difference in macrophages vs neutrophils

A

-Macrophages: phagosome is merged with lysosome
-Neutrophils: pathogens are killed by antibacterial compounds and enzymes found in primary and secondary granules

49
Q

Macrophage digestion

A

-oxygen-dependent
-Damages DNA, RNA, and proteins
-uses reactive oxygen species (superoxides, peroxides, hydroxyl radicals), nitrous oxide, and hypochlorous ions
-long lifespan

50
Q

Neutrophil digestion

A

-oxygen-independent
-membrane or cell wall disruption
-uses lysozyme, lactoferrin, and antimicrobial peptides
-after digestion, neutrophils self destruct and release DNA and other fibers to create a sticky antimicrobial NET (neutrophil extracellular trap)

51
Q

How does the body handle large protozoan parasites?

A

Use neutrophils and eosinophils that can kill pathogens by excreting toxic compounds and enzymes in primary and secondary granules

52
Q

Degranulation

A

The release of antimicrobial cytotoxic from granules from inside some cells, works via membrane or cell wall disruption

53
Q

Enhanced destruction with ________________

A

the complement system

54
Q

Complement System

A
  1. Enhance inflammation
  2. Help macrophages engulf pathogens (opsonization)
  3. Form a membrane attack complex, leading to pathogen lysis
    *classical pathway or lectin pathway
55
Q

Opsonization

A

-part of the complement system
-the coating of pathogens w/ antibodies, complement proteins, or other proteins to facilitate binding of phagocytes and NK cells
-phagocyte membrane receptors recognize and bind to C3b that activate opsonization

56
Q

Lectin Complement Pathway

A

-grab hold of a pathogen
1. Receptor binding
2. Actin-driven protrusion
3. Coupling actin to the surface
4. Membrane delivery
5. Membrane fission

57
Q

Form a membrane attack complex

A

-last step of complement system
-destabilizes the plasma membrane of pathogen

58
Q

What two things do NK cells look for?

A
  1. Activation
  2. Inhibition
59
Q

Activation of NK cells

A

proteins on surface of target cell that allow the NK cell to bind and kill

60
Q

Inhibition of NK cells

A

protein (MHC I) on surface of infected/tumor cell that signals if a cell is healthy or not

61
Q

If MHC I molecule on tumor cell matches Inhibitory KIR receptor on NK cell?

A

No killing

62
Q

If MHC I molecule on tumor cell doesn’t match Inhibitory KIR receptor on NK cell?

A

Killing

63
Q

Strong inhibition of NK cells

A

Healthy, “normal” cells express enough MHC I molecules to induce a strong inhibitory signal in NK cells and are protected from NK cell attack

64
Q

Reduced inhibition of NK cells

A

Tumor or infected cells often downregulate MHC I molecule and can no longer deliver a strong inhibitory signal, so NK cells can overpower the signal and attack and eliminate these cells

65
Q

Strong activation of NK cells

A

-Transformed or infected cells sometimes increase the expression of molecules that are recognized by activating NK cell receptors
-Result: NK cells receive a stronger activating signal than usual and can override inhibitory signal and attack

66
Q

What two proteins do NK cells use to kill target cells?

A
  1. perforin: creates a controlled pore in the target cell to deliver granzymes
  2. granzymes: enzyme that activates apoptotic enzymes to induce apoptosis

BSCI 2150 (11 decks)

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