Innate Immune Recognition and Effector Mechanisms Flashcards

(65 cards)

1
Q

PAMP abundance, prevalence, absent in what tissues?

A

Abundant, essential molecules
Common to many microbes
Absent from host tissues

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2
Q

PAMP Gram positive bacteria example?

A

peptidoglycans

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3
Q

PAMP gram negative bacteria example?

A

lipopolysaccharide

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4
Q

PAMP virus example?

A

dsRNA

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5
Q

What are the signaling types of PRRs?
Describe location and examples.

A

Toll like receptors- membranous, wide variety of ligands
NOD like receptors- cytoplasmic, peptidoglycan
RIG 1 like receptors- cytoplasmic, viral dsRNA

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6
Q

Where are pattern recognition receptors (PRRs) found?

A

Cell surface
Cytoplasmic
Endosomal
Soluble

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7
Q

Where are TLRs 4 and 5 located and function?

A

plasma membrane
recognize bacterial, fungal, parasite wall components

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8
Q

TLRs 3, 7, 8, 9 location and function?

A

Endosomal membrane, recognize bacterial/viral RNA, DNA

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8
Q

Write out the 4 components of PRR signaling?

A

Slide 8

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9
Q

IBD is common in what breed?
Why?
Result?

A

German shepherd
polymorphisms of TLR4 and TLR5 genes
Reduced ability to defend against bacteria in intestine

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10
Q

Why does normal flora in the gut not trigger enteritis?

A

TLR5 recognizes flagellin

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11
Q

Describe leaky gut syndrome?

A

Activation of normal flora

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12
Q

Where are NOD like receptors located, recognize what, signal through?

A

cytosol
peptidoglycan
NF-kB

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13
Q

Where are RIG-1-like receptors, recognize, activate, expression of?

A

cytosol
recognizes dsRNA and ssRNA
activates nF-KB
expression of type I IFNs

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14
Q

What do phagocytic receptors trigger?

A

Phagocytosis

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15
Q

Phagocytic Complement receptor recognizes?

A

microbes coated with complement components

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16
Q

Phagocytic FcyR recognizes?

A

microbes coated with IG

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17
Q

Phagocytic mannose receptor recognizes?

A

sugar residues on microbes

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18
Q

In opsonization, C3b is recognized by Complement Receptor __ and __ (____).

A

1 and 3 (CR1 and CR3)

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19
Q

In opsonization, what is IGG recognized by?

A

FcYr

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20
Q

Draw and write out phagocytosis part II.

A

Slide 20

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20
Q

What action is more efficient phagocytosis than through PRRs alone?

A

opsonization

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21
Q

Write out the 4 steps of phagocytosis.

A

Slide 19

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22
Q

What produces mannose-binding lectin? Activates?

A

liver, CS

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22
Draw and write out phagocytosis part III.
Slide 21, 22, 23
23
C-reactive major what? Produced by? Activates?
acute phase protein liver activates complement, enhances phagocytic clearance
24
How does the immune system recognize when self is damaged?
Stimulate immune response to clean up Pathogenic tissue causes cell and tissue injury
25
What does the immune system release in response to cell injury?
releases cytosolic/nuclear proteins and metabolites
26
What does the immune system release in response to tissue injury?
extracellular matrix components
27
Two types of DAMPs?
Intracellular and extracellular
28
5 results of PRR signaling?
Phagocytic activation, cytokines, chemokines, adhesion molecules, lipid mediators
29
What does phagocyte activation do?
upregulation of respiratory burst enzymes, phagocytic receptors, antigen presenting molecules
30
Cytokine function?
Induce production of more leukocytes Start inflammatory cascade
31
Chemokine function?
Leukocyte recruitment
32
Adhesion molecule function?
Allow leukocytes to stop and migrate from blood to tissues
33
Lipid mediator function?
Arachidonic acid cascade Platelet activating factor
34
How do sentinel cells recognize and respond to PAMPs and DAMPs?
engagement of PRRs
35
Three PRRs?
TLRs NLRs RLRs
36
Ligand binding results in activation of ___ or _____. Thus, _______________
NF-KB or IRF transcription of genes involved in inflammation
37
Phagocytic PRRs trigger ________ thus _____________ involving enzymes, low pH, free radicals
engulfment of microbes phagolysosomal degradation
38
Recognition of PAMPs and DAMPs triggers the formation of the _________ thus activation of _____ and _____.
inflammasome IL1B and IL18
39
NETS type of process?
active
40
NETs respond to ______ and _______.
IL 8 and PAMPS
41
NETS composed of? (what is super sticky)
DNA- super sticky Histones Elastase Defensins Myeloperoxidase
42
Actinobacillus pleuropneumoniae causes what? Presentation?
severe pleuropneumonia in dogs Well demarcated areas of necrosis bordered by neutrophils and NETS
43
What is a major basic protein? Cytotoxic for what?
Eosinophil; helminths
43
Eosinophil cationic protein function?
Pore-forming in membranes Digests RNA
44
Eosinophil derived neurotoxin function?
Ribonuclease with antiviral properties
45
Eosinophil peroxidase function?
Oxidative damage via H2O2
46
NADPH oxidase on plasma membrane function?
oxidative burst
47
What are the two types of receptors of NK?
Activation and Inhibitory receptors
48
Function of activation receptor?
recognize viral proteins, altered surface glycoproteins , antibody coated cells
49
Function of inhibitory receptor?
recognize normal MHC class I expressed on all nucleated cells, marker of self , overrides activation signaling
50
If the inhibitory signal is absent then ______________.
releases lytic granules
51
Where does perforin insert?
membrane
52
Where does granzyme enter and trigger?
pore and apoptosis
53
What are the 3 effector mechanisms of the innate immune system? Importance of each?
1. Phagocytosis and degradation - extracellular and intracellular infections 2. Extracellular granule release- extracellular and helminth infections 3. NKC targeted cytotoxicity- viral infections and cancer
54
Phagosomal maturation is the process of ______________ and ________________.
acidification and fusion with lysosomes respiratory burst
55
Uric acid is a _________.
DAMP
56
Any treatment that blocks IL1 will make pt
prone to infection
57
Inflammasome activates
IL1
58
What is systemic lupus erythematosus?
Slide 43
59
Connection between PRRs and vaccination?
receptors
60
TLRs and cancer connection?
See slide 45
61
Write out slide 46.
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