Immuno 11: Innate Immunity Flashcards

1
Q

Parasites are a group of disease-causing agents that include ____ and ____.

A

worms and protozoa

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2
Q

The tremendous diversity of pathogens has led the immune system to develop 2 critical features. They are:

A
  1. specific BCRs and TCRs of equal or greater diversity than pathogens
  2. wide range of distinct effector mechanisms to combat the pathogens
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3
Q
Pathogens that remain in extracellular locations are best combated by \_\_\_\_
immune responses (complement fixing and neutralizing Ab isotypes) and by \_\_\_\_.
A

humoral; phagocytosis

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4
Q

Pathogens that grow in the cytoplasm of cells (intracellularly) are cleared primarily by ____ and ____ cells.

A

CTLs and NK cells

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5
Q

Protection against pathogens that grow in vesicles of phagocytes (intracellularly) is mediated primarily by ____-mediated
activation of ____.

A

T cell-mediated

activation of macrophages

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6
Q

Direct methods of tissue damage include __________, whereas indirect mechanisms involve ________.

A

production of exotoxins and endotoxins, and direct cytopathicity of host cells; innate and acquired immune responses of the host

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7
Q

What is molecular mimicry?

A

indirect mechanism of tissue damage wherein pathogen elicits antibodies specific for host cell proteins

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8
Q

Cryptidins/defensins are ____ ____ produced by ____ cells (lining the small intestine) and by
____.

A

antibacterial peptides; Paneth cells and neutrophils

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9
Q

How do amphipathic peptides attack bacteria?

A

they insert into their outer envelope and disrupt their integrity

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10
Q

What prevents bacteria from colonizing in the stomach

A

acid and hydrolytic enzymes

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11
Q

What component of tears and saliva degrades bacterial cell walls?

A

lysozyme

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12
Q

What are the two main mechanisms by which normal flora are a defense against pathogens?

A
  1. they compete for attachment to epithelial cells, and nutrients
  2. they produce antibacterial proteins called colicins
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13
Q

If it’s true that complement component C3 is constantly activated at low level in the blood, how does it respond to an infection?

A

the rate of C3 cleavage increases in the vicinity of some pathogens; also when C3 is cleaved it is rapidly degraded unless a pathogen is present for it to bind to

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14
Q

Factor __ binds to the C3 convertase to stabilize it by preventing Factor __ from dampening the complement activation cascade.

A

Factor P (properdin); Factor H

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15
Q

Please name the host cell surface proteins that prevent the complement cascade from marking them for uptake and destruction.

A
  • CR1
  • DAF
  • MCP
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16
Q

What host cell surface proteins interfered with MAC formation on host cells?

A

CD59 (protectin)

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17
Q

Is factor H a plasma protein or a cell surface protein? What does it do?

A

plasma protein; it renders C3 convertase susceptible to cleavage by factor I in the process of protecting host cells from complement destruction

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18
Q

What 2 cells initiate the inflammatory response and provide innate cell-mediated immunity (CMI)?

A

macrophages and neutrophils

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19
Q

Macrophages and neutrophils have what 2 receptors on their surface that allow them to recognize/phagocytose bacterial material?

A
  1. PRRs - recognize PAMPs

2. complement receptors - recognize opsonized material

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20
Q

Once pathogens are ingested, what agents do macrophages/neutrophils produce to kill or deactivate the pathogen?

A
  • acid
  • toxic oxygen derivatives
  • antibacterial peptides/proteins
  • competitors
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21
Q

Big duties of macrophages include releasing ____, ____, and to act as ____.

A

cytokines, phagocytosis, professional APCs

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22
Q

What is considered the first of a series of reactions known as the imflammatory response?

A

arrival of neutrophils at the site

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23
Q

Neutrophils are specialized for working under ____ conditions.

A

anaerobic

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24
Q

How long do neutrophils survive after entering inflamed tissue, and what happens to their dead cell body?

A

they survive about 5-6hrs; the dead cells form pus

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25
Q

True or false: the neutrophil’s granules are formed upon phagocytosis of a pathogen.

A

False - they are pre-formed and ready to fuse with the phagosome

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26
Q

What are the contents of a neutrophil granule?

A

hydrolytic degradative enzymes, NADPH-dependent oxidases, and antimicrobial peptides (defensins)

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27
Q

What do NADPH-dependent oxidases generate?

A

they generate toxic oxygen radicals (superoxide, hydroxyl oxide, and hydrogen peroxide), which give rise to hypochlorous acid (HOCl)

28
Q

What is the respiratory/oxidative burst?

A

this is the oxidative attack (production of toxic oxygen radicals) mounted by neutrophils on pathogens; can kill Gram positive and negative bacteria, fungi, and some enveloped viruses

29
Q

True or false: once neutrophils empty all their granules, they will make more.

A

False - once neutrophils empty all their granules, they die, hence their short lifespan and all the pus

30
Q

True or false: once macrophages empty all their lysosomal contents, they will make more.

A

True - this is how macrophages can live so long

31
Q

What is netosis?

A

it’s the process by which neutrophils die while making a NET (neutrophil extracellular trap) that immobilizes pathogens; they expel their chromatin to form the NET and their antimicrobial molecules that attack pathogens caught in the NET

32
Q

What are the 3 types of PRRs?

A
  1. endocytotic PRRs
  2. signaling PRRs
  3. secreted PRRs
33
Q

True or false: endocytotic PRRs promote the attachment, engulfment, and destruction of pathogens by using intracellular signaling.

A

False - this is all done without intracellular signaling

34
Q

What do endocytotic PRRs primarily recognize?

A

carbohydrates

35
Q

Mannose receptors are an example of ____ PRRs and are present on ____.

A

endocytotic; macrophages

36
Q

What kind of endocytotic PRR recognize charged ligands, and on what cells are they found?

A

scavenger receptors; found on all phagocytes

37
Q

What is a glucan receptor?

A

an endocytotic PRR that is found on all phagocytes

38
Q

Signaling PRRs include the large families of what two receptors?

A
  1. TLRs (toll-like receptors) - membrane bound

2. NOD-like receptors - cytoplasmic

39
Q

TLRs recognize microbial constituents such as …?

A

LPS, CpG, DNA motifs, DS DNA, flagellin, proteoglycans

40
Q

Once TLRs recognize their ligand, they initiate production of what?

A

cytokines - by way of several TLRs associating on the cell surface and initiating an intracellular signaling cascade to the nucleus

41
Q

____ is the only TLR that is known to bind directly to its ligand, which is ____.

A

TLR-5; flagellin

42
Q

Current understanding of NOD-like receptors is what?

A

these proteins have affinity for microbial products, and when they bind they initiate signaling in production of inflammatory cytokines

43
Q

What are secreted PRRs?

A

PRRs that are secreted from host cells. DUH.

44
Q

What are some examples of secreted PRRs?

A

MBL, complement receptors, collectins, serum amyloid, CRP, lipid transferases, and peptidoglycan recognition proteins (PGRs)

45
Q

What pathogen surface groups does MBL recognize/bind?

A

sugar groups (predominantly), phospholipids, nucleic acids, and non-glycosylated proteins

46
Q

Once MBL binds a pathogen, what happens next?

A

MASP-1 and -2 bind MBL

and these MASPs cleave C2 and C4; the products go on in the lectin complement pathway

47
Q

C-reactive protein (CRP) binds to ____ on pathogens and then becomes a ligand for ___.

A

phospholipids; C1q

48
Q

MBL and CRP are both what type of PRR?

A

secreted PRRs

49
Q

What is the timeline for immune response to infection?

A
  1. innate - 0-4hrs after encounter
  2. early adaptive - 4-96hrs; will respond if the innate system is overwhelmed/evaded
    3.
50
Q

True or False: early adaptive responses involve recognition mechanisms that are based on relatively invariant receptors and do
not lead to lasting protective immunity.

A

True

51
Q

What is the usual role of the early adaptive immune response?

A

to hold the bacterial infection in check until adaptive immune responses have formed

52
Q

An important function of the innate immune response is to recruit more ____ and ____ ____ to the site of infection.

A

phagocytes; effector molecules

53
Q

____ release a variety of molecules that are involved in the inflammatory response.

A

phagocytes

54
Q

Inflammatory responses are characterized by ____, ____, ____, and ____.

A

pain, redness, heat, and swelling

55
Q

TNF-α (produced by phagocytes) indirectly induces ____ in the small local vessels (in area of inflammation); this occludes the vessels, thereby preventing flow of blood; this helps to ____ of the pathogen through the bloodstream.

A

blood clotting; prevent dissemination to other regions of the body

56
Q

TLR__/TLR__ heterodimers recognize lipoteichoic acid (‘LTA’, a component that is common to gram-positive bacteria) and zymosan (a component of fungi).

A

TLR2/TLR6
(Aid: 2 and 6 are 2 different “guys”, so two “lines” in Gram +, or they recognize 2 different guys: Gram+ bacteria and fungi)

57
Q

True or False: TLR5 bind to double-stranded viral RNA.

A

False - it’s TLR3

Aid: thREE - R = RNA, EE = double stranded, “three” = TLR 3

58
Q

TLR4 homodimers serve as a receptor for ____.

A

LPS (lipopolysaccharide, a component found on gram-negative bacteria)
(Aid: 4 and 4 are the same “guys”, so one “line” in Gram -)

59
Q

Which TLR(s) recognize single-stranded viral RNAs?

A

TLR7 and TLR8

Aid: they don’t dimerize, they’re single-strands

60
Q

What are the major end products of the acute phase response?

A
  • liver secretes PRRs (MBL/CRP) to activate complement and opsonize pathogens
  • recruitment and activation of phagocytes
  • fever
61
Q

What are the 3 cytokines most responsible for initiating the acute phase response?

A

IL-1, IL-6, TNF-alpha

62
Q

How does sepsis lead to organ failure?

A

when a bacterial infection becomes septic, TNF-alpha is secreted systemically; this still has the effect of activating platelet adhesion, which can cause small vessels to occlude/collapse; this is particularly problematic in some organs, because it can cause them to fail/septic shock/death

63
Q

Problems fighting a Gram-positive bug could be attributed to deficiency of which TLR(s)?

A

TLR2/6

64
Q

Problems fighting a Gram-negative bug could be attributed to deficiency of which TLR(s)?

A

TLR 4

65
Q

Which TLR(s) would be effective against parasites? (because they recognize GPI)

A

TLR1/2 heterodimer

66
Q

The TLR1/2 heterodimer will bind ____ and ____.

A

lipopeptides (component of bacteria) and GPI (component of parasites)

67
Q

TLR9 binds ____ in ____ and ____.

A

unmethylated CpG-rich DNA in bacteria and viruses