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Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

when does the innate immune response begin?

A

immediately when pathogen is encountered with virtually no delay

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2
Q

what are the 2 types of external barriers of the innate immune system?

A
  1. epithelial barriers

2. antimicrobial proteins/peptides that are secreted

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3
Q

give 4 examples of epithelial barriers of the innate immune system

A
  1. skin
  2. lining of respiratory tract
  3. lining of GI tract
  4. lining of urogenital tract
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4
Q

give 7 examples of secretions from tissues in the innate immune system

A
  1. tears
  2. mucus
  3. sweat
  4. HCl in stomach
  5. urine
  6. milk from mammary glands
  7. saliva
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5
Q

give 3 antimicrobial proteins/peptides of the innate immune system

A
  1. lysozyme
  2. defensins
  3. surfactants
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6
Q

what do innate immune cells have and what do they do?

A

innate immune cells have PRRs that bind to PAMPs

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7
Q

when the PRRs of innate immune cells bind to pathogen PAMPs, what does it ressult in? (2)

A
  1. induction of gene expression always

2. sometimes induction of phagocytosis

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8
Q

what are the 5 types of PRRs of the innate imune system?

A
  1. Toll-like receptors (TLRs)
  2. Lectin receptors
  3. scavenger receptors
  4. cytosolic innate receptors
  5. opsonin receptors
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9
Q

what do lectin receptor PRRs do?

A

bind to carbohydrates

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10
Q

where are cytosolic innate receptor PRRs found?

A

inside the cell! good second line of defense

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11
Q

what do opsonin receptor PRRs do?

A

bind to opsonin when the opsonin is bound to a pathogen

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12
Q

PRRs binding to PAMPs can result in what? (6)

A
  1. induction of antimicrobial proteins: defensin is major
  2. induction of Type I IFNs
  3. induction of pro-inflammatory cytokines: IL-1, IL-6, and TNF-a
  4. induction of chemokines: IL-8
  5. induction of enzymes
  6. initiation of phagocytosis
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13
Q

what are the 3 major pro-inflammatory cytokines that aare induced after PRRs bind to PAMPs?

A

IL-1, IL-6 and TNF-a

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14
Q

what is the major chemokine induced after PRRs bind to PAMPs?

A

IL-8

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15
Q

what does induction of enzymes after PRRs bind to PAMPs do?

A

results in synthesis of products that are either anitmicrobial or mediators of inflammation

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16
Q

when PRRs bind to PAMPs, do all 6 possible results occur?

A

not always, but it is possible

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17
Q

give the 6 steps of phagocytosis

A
  1. cell surface receptor recognizes a pathogen
  2. this results in polymerization of actin microfilaments which extend the cell membrane to engluf the pathogen
  3. pathogen is internalized in a phagosome
  4. phagosome fuses with lysosomes inside the cell (if cell is a neutrophil, phagosome also fuses with cytoplasmic granules)
  5. lysosomes (and granules of neutrophils) contain anti-microbial agents that kill pathogen
  6. pieces of pathogen that are left are released from the cell
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18
Q

what are the 2 methods of initiation of phagocytosis?

A
  1. Direct: PAMP recognition by PRR

2. Indirect: opsonins bind to pathogens and mark them for phagocytosis, cells recognize the OPSONIN, not the PATHOGEN

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19
Q

what is released when lysosomes fuse with the phagosome? (4)

A
  1. anti-microbial peptides/proteins (defensins)
  2. proteases (enzymes)
  3. acidic agents (to lower pH)
  4. molecules that mediate oxidative damage (to damage lipid of cell membrane)
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20
Q

what are the 2 methods of microbe degradation/oxidative damage to kill pathogens?

A
  1. oxidative damage caused by reactive oxygen species (ROS)

2. oxidative damage caused by reactive nitrogen species (RNS)

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21
Q

give 3 reactive oxygen species (ROS)

A
  1. superoxide anion (O2-)
  2. H2O2
  3. HClO
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22
Q

what is the role of superoxide anion?

A

(-) allows O to bind to lipids

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23
Q

what is the active component of bleach that is found in the body!!

A

HClO

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24
Q

what is the reactive nitrogen species that kills pathogens?

A

NO

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25
Q

when are reactive oxygen and nitrogen species made and why?

A

made only once lysosome fuses with phagosome because don’t want floating around in the body

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26
Q

what happens to the reactive oxygen and nitrogen species once they have done their job?

A

they are released into the environment, will damage some healthy tissue, but then that tissue is cleaned up and regenerated

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27
Q

describe the 4 step process of neutrophil extracellular traps killing pathogens (bad as fuck)

A
  1. PAMPs bind to specific PRRs on neutrophils
  2. neutrophils will expel chromatin outside of the cell and the chromatin is accompanied by cellular antimicrobial agents
  3. expelled chromatin traps pathogens, resulting in their death
  4. neutrophil will die via NETosis
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28
Q

how far can NETs extend from the cell?

A

10-15 times the length of the cell

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29
Q

what 5 symptoms are characteristic of the inflammatory response?

A
  1. swelling
  2. redness
  3. heat
  4. pain
  5. loss of function
30
Q

guve the 5 step process of the inflammatory response

A
  1. tissue is infected or injured
  2. tissue-specific macrophages and dendritic cells will recognize pathogen and phagocytose it (the true first responders)
  3. PAMPs binding to PRRs also initiate release of hemokines and pro-inflammatory cytokines (IL-6, IL-1, and TNF-a)
  4. release of pro-inflammatory cytokines causes: increased vascular permeability and vasodilation
  5. chemokines (IL-8) attract other cells to site of infection
31
Q

what does the increased vascular permeability caused by the pro-inflammatory cytokines in the inflammatory response do?

A

makes it easier for cells to leave bloodstream

32
Q

what does the vasodilation caused by the pro-inflammatory cytokines in the inflammatory response do?

A

allows for increased blood flow and causes swelling, redness, and heat

33
Q

name 2 types of cells that are always attracted to the site of infection by chemokines in the inflammatory response and 3 that willbe attracted if a parasitic infection

A
  1. neutrophils
  2. monocytes leave bloodstream and differentiate into macrophages
  3. mast cells, eosinophils, and basophils if parasitic
34
Q

who are the first responders from the BLOODSTREAM in the inflammatory response?

A

neutrophils

35
Q

how do neutrophils assist in the inflammatory response after being attracted by chemokines?

A
  1. those that leave the bloodstream begin phagocytosis

2. and release the contents of their cytoplasmic granules

36
Q

once monocytes leave the bloodstream and differentate into macrophages in response to chemokines, what do they do?

A

perform phagocytosis of noth antigen and damaged tissue (cleanup crew)

37
Q

what is the acute phase response?

A

the phase preceding recovery or death

38
Q

give 6 symptoms experienced in the acute phase response and what those are cuased by

A
  1. increase in hematopoeisis
  2. fever
  3. lethargy
  4. muscle pain
  5. loss of appetite
  6. metabolic changes
    caused by systemic effects of proinflammatory cytokines
39
Q

what causes the increase in hematopoeisis observed in the acute phase response?

A

cytokines act on bone marrow to increase production of immune cells; act on specific cells for infection type (like basophils and eosinophils in parasitice infections)

40
Q

what causes the fever observed in the acute phase response? (2)

A
  1. IL-1 results in cyclooxygenase (COX2) production in the brain which stimulates prostaglandin production, which causes body temperature to rise
  2. animals shiver to increase metabolism, resulting in heat production
41
Q

what is the function of fever that is observed in the acute phase response?

A

the increase in body temperature enhances immune cell function and decrease in apoptosis of immune cells (get back to work you bitches you’re not allowed to die)

42
Q

what causes the lethargy observed in the acute phase response?

A

pro-inflammatory cytokine act on brain to promote release of sleep-mediating molecules

43
Q

what is the function of the lethargy observed in the acute phase response?

A

to conserve energy

44
Q

what causes the muscle pain observed in the acute phase response?

A

cytokines act on sensory nerves to stimulate pain

45
Q

what is the function of the muscle pain observed in the acute phase response?

A

also energy conservation; less likely to move if it hurts

46
Q

what causes the loss of appetite observed in the acute phase response? potential function?

A

cytokines act on hunger centers in the brain to decrease appetite; potentially to starve out the pathogen

47
Q

what causes the metabolic changes observed in the acute phase response?

A

cytokines act on muscle to stimulate catabolism of protein

48
Q

what is the function of the metabolism changes observed in the acute phase response? (2)

A
  1. supplies amino acids for immune cell protein production and
  2. for protein production in the liver
49
Q

what is the reason for acute phase protein production in the liver?

A

they are used as markers

50
Q

name two iron binding proteins produced in the liver during the acute phase response and describe their function

A
  1. transferrin
  2. haptoglobin
    bind iron and make it unavailable to the bacteria who need iron to survive
51
Q

in retaliation to production of transferrin and haptoglobin in the liver during the acute phase response, what do bacteria produce and what does it do?

A

bacteria produce siderophores that remove iron from transferrin and haptoglobin for bacterial use

52
Q

in retaliation to the bacterial production of siderophores, what does the liver then produce in the acute phase response and what does it do?

A

liver produces lipocalin-2, which binds siderophores, preventing them from binding iron

53
Q

is there any growth during the acute phase response? what impact does this have on livestock?

A

no growth during the acute phase response, which impacts production and specifically broilers so intensely that they take longer to reach market weight if they experience this response

54
Q

can viruses be recognized by PRRs outside the cell? why or why not?

A

no! viruses attack by invading and hijacking host cells

55
Q

what specific PRR recognizes viruses?

A

cytosolic innate receptors inside the cell

56
Q

what des cytosolic innate PRR recognition of viral pathogens cause? (2)

A
  1. secretion of IFNA and IFNB

2. secretion of proinflammatory cytokine

57
Q

what is the result of secretion of IFNA and IFNB following cytosolic innate PRR recognition of viruses? (2)

A
  1. prevents viral replication

2. increase MHC expression

58
Q

what is the result of secretion of proinflammatory cytokines following cytosolic innate PRR recognition of viruses?

A

TNF-a activate NK cells

59
Q

what is the only cell of the innate immune system that can kill infected cells, not just phagocytose them?

60
Q

what are the 2 types of receptors on NK cells?

A
  1. inhibitory receptors

2. activating receptors

61
Q

what are the 2 functions of the inhibitory receptors on NK cells?

A
  1. recognize MHC I

2. inhibit cytotoxic activity of the NK cell

62
Q

what are the 2 functions of activating receptors on NK cells?

A
  1. recognize activating ligands on infected cells

2. stimulate cytotoxic activity of the NK cell

63
Q

when NK cells receive more inhibitory signals than activating signals from a cell, what is the result?

A

NK cell will not kill the healthy cell

64
Q

when NK cells receive more activating than inhibitory signal from a cell, what is the result?

A

NK cell will kill the altered or infected cell

65
Q

where do inhibitory signals for NK cells come from on potential target cells?

A

from MHC I complex

66
Q

whhere do activating signals for NK cells come from on potential target cells?

A

from activating ligands

67
Q

what are the 2 ways/scenarios that an NK cell can be activated?

A
  1. viruses inhibit MHC expression on infected cells, so inhibitory receptors cannot bind MHC, so NK cell receives more activating signals, stimulating cytotoxic activity
  2. stressed (infected) cells increase expression of activating ligands, so NK cell activating receptors have more activating ligands to bind which will stimulate more cytotoxic activity
68
Q

what are the 2 ways that NK cells kill?

A
  1. NK cells express FasLigand (FasL); direct cell-to-cell contact
  2. NK cells secrete perforin and granzyme
69
Q

describe how NK cells kill by expressing FasLigand (FasL)

A

FasL binds Fas on infected cells, resulting in apoptosis

70
Q

desscribe how NK cells kill by secreting perforin and granzyme

A
  1. perforin embeds in cell membranes, resulting in perforation in that membrane, which will eventually kill the cell, but can be aided by
  2. granzyme, which enters the cell and activate apoptosis
71
Q

as they are killing, what do NK cells also secrete and what does it do? (3)

A

IFN-gamma, which

  1. stimulates macrophages
  2. macrophages “clean up” cellular damage
  3. activate the adaptive response~

Immunology (13 decks)

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