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MIC 420 > Exam 1 > Flashcards

Exam 1 Flashcards

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1
Q

Non Vertebrates Immunity

A

All mammlas, fish, insects, and even bacteria have an innate immunity

Without circulatory sytem, adaptive surveillance is a problem

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2
Q

Vetrebrates

A

Innate immune system provides first line of protection, and informs the adaptive immune system to respond

recognition results in pro-inflammatory response to activate B/T cells type of recognition instructs the appropriate adaptive response

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3
Q

Opportunistic infections

A

occur when microbes gain cross epithelia
barriers

Cystic Fibrosis: defective chloride channel (CFTR) results in inefficient clearance of mucous to digestive tract (oral toilet), leading to chronic bacterial infection in lung and systemic infections

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4
Q

Example of opportunistic infection

A
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5
Q

PAMPS

A

Microbial structures that are recognized by
innate immune system receptors are called
Pathogen Associated Molecular Patterns

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6
Q

Innate Receptors that recognize PAMPs are
called

A

Pattern Recognition Receptors (PRRs)

PRR recognition of PAMPs results in a
stereotyped response tailored to the type of
microbe that has that PAMP.

PRR/PAMP system maintains both self/nonself
discrimination and allows responses to be
tailored to the type of infecting microbe

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7
Q

LPS

A

anti-bacterial response

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8
Q

dsRNA

A

anti-viral response

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9
Q

Mutation of PAMPs

A

would incur significant cost
microbe (replication, altered structure/function)

For yeast, bacteria – unique lipid/carbohydratemoieties not found on host cells

For viruses – unique nucleic acids (non-host)

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10
Q

Scavenger receptors

A

recognize extracellular
anionic polysaccharides and lipoproteins of
gram positive bacteria

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11
Q

Lectins

A

recognize extracellular
polysaccharides of fungal cell walls

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12
Q

Toll Like Receptors (TLR)

A

recognize
extracellular and endosomal components
from many microbes

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13
Q

RIG-I Like Receptors (RLR)

A

recognize
intracellular nucleic acids from virus (and
some bacteria)

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14
Q

NOD Like Receptors (NLR)

A

recognize
intracellular imbalances due to infection

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15
Q

Different groups of PRR

A
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16
Q

Scavenger Receptors

A

recognize extracellular
anionic polysaccharides and lipoproteins

Involved in both host maintenance (scavenger function) and microbe recognition (innate immune function)

Host: recognize low density lipoproteins, high
density lipoproteins, and hemoglobin (from
RBC)

Microbe: recognize components of gram
negative bacterial cell wall

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17
Q

Scavenger receptors groups

A
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18
Q

Lectins

A

recognize extracellular polysaccharides on free proteins (scavenger), host (cell signaling) or microbes (innate recognition)

Scavenger: glycoproteins are recognized,
broken down in endosomes, and reused

Host: cell to cell contact and adhesion,signaling

Microbe: polysaccharides on bacteria cause
cross linking and activation of innate pathways

Also Mannose binding lectin complement
pathway

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19
Q

Lectins in Innate Immune Activation

A
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20
Q

Discovery of Toll Like Receptors

A

Christiane Nusslein-Volhard showed that Toll proteins direct embryonic cell differentiation in fruit flies

Jules Hoffman showed different Toll genes conferred resistance to fungi vs. bacteria; some Toll mutants were susceptible to fungal infection but had normal resistance to bacteria

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21
Q

Toll Like Receptors Recognize Bacterial LPS

A

Bruce Beutler showed C3H mice have a mutation in LR4 that made them resistant to LPS, but unable to control live bacterial infection.

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22
Q

Recognizes triacyl lipoproteins, glycolipids, lipoteichoic acid (gram+ bacteria), zymosan (fungi), HSP70 (host), others…

A

TLR 1 and 2

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23
Q

TLR 2 and 6:

A

recognizes diacyl lipoproteins, along with other TLR1/2 ligands.

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24
Q

TLR 3:

A

recognizes double stranded RNA (viruses, some bacteria)

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25
Recognizes lipopolysaccharides (LPS) (bacteria)
TLR 4 (w/MD-2)
26
TLR 5:
recognizes flagellin (bacteria)
27
TLR 6:
recognizes lipopeptides (mycoplasma)
28
Recognizes ssRNA (viruses):
TLR 7 and 8
29
Recognizes CpG motifs in dsDNA (viruses, some intracellular bacteria)
TLR 9
30
TLR 10:
recognizes unknown ligand
31
TLR 11 and TLR 12:
recognize profilin (toxoplasma)
32
Recognizes ribosomal RNA (bacteria, some viruses)
TLR 13
33
Mammals have Humans: mice: Drosophila: Sea Urchin:
10-15 different TLR 10 TLR (no 11-13) 12 TLR (no 10) have 9 different TLR have 222 different TLR
34
Ruslan Medshitov and Charles Janeway
showed that a constitutively active human homolog of Toll (TLR4) induced inflammatory cytokines in human cells. (Nobel Prize 2011)
35
Extracelluar TLR
recognize intact structures on bacterial, fungal, (parasite?) ligands. TLR 1, 2, 4, 5, 6, 11, 12
36
Intracellular TLR
are expressed in endosomes and recognize nucleic acids from degraded pathogens (primarily viruses). TLR 3, 7, 8, 9, 13
37
RIG-I Like Receptors (RLR) and NOD Like Receptors
are expressed in the cytoplasm to recognize intracellular bacterial and viral products
38
Compartmentalization of Toll Like Receptors
39
What signal is mainly used for most TLR signals?
MyD88 protein
40
TLR3 signals through:
the TRIF protein (main signal is via IRF3)
41
TLR4 can signal through:
either MyD88 orTRIF proteins (main signal is via NFκB)
42
Depending on which TLR is activated, different types of inflammatory responses are initiated to tailor the response to the type of pathogen being recognized. Further directed by the type of cell expressing the activated TLR.
43
Mice deficient in any one TLR are rarely susceptible to microbial infection
Mice deficient in MyD88 are susceptible to bacterial infection Mice deficient in TRIF are susceptible to some viral infections (herpesviruses)
44
Some of the main cytokines produced in response to TLR signals:
Tumor Necrosis Factor (TNF) - general inflammation inflammation, cell recruitment, cell death Interleukin 12 (IL-12) – immune responses to extracellular pathogens inflammation, initiation of adaptive response Type I Interferons (IFN) – immune responses to intracellular pathogens poise cells for infection, initiation of adaptive response Interleukin 6 (IL-6) – general effects acts on hypothalamus increase body temperature
45
Cellular consequences of TLR signals
1. stop pinocytosis/phagocytosis – already have recognized (and internalized) microbe. Ensures that response is only to that specific microbe. 2. increase expression of MHC and costimulatory proteins to become ready to stimulate adaptive immune response 3. decrease expression of adhesion molecules that retain in periphery to migrate to draining lymph nodes.
46
Shizuo Akira
showed that RIG-1 protein bound dsRNA and triggered an inflammatory response (IFN).
47
Michael Gale Jr.
showed that RIG-1 protein made cells resistant to viral infection.
48
Similar to TLR proteins, RIG Like Receptors (RLR) crescent shaped α-helical domains to bind ligands
All identified RLR bind intracellular nucleic acids from viruses (and some bacteria) mammals have 8 known RLR
49
RIG-I Like Receptor Signaling
Most RLR signal through the IPS-1, an adaptor protein on mitochondria. Signaling intermediates are similar to those in TLR pathway: NFκB and IRF3 Main result is production of type I interferons (IFN). IFNs make infected and surrounding cells non-permissive for virus growth (same as for TLR induced IFN). Dendritic cells migrate to draining lymph nodes and stimulate adaptive immune response.
50
Pathway of RIG-I Like Receptor Signaling
51
IFN makes surrounding cells poised for infection
IFN binding to IFN-Receptor increases expression of Protein Kinase R (PKR) and 2’-5’ oligoadenylate synthetase (OAS) Binding of dsRNA to PKR results in activation, then phosphorylation and inactivation of eIF-2α to shut down protein synthesis Binding of dsRNA to OAS converts ATP to 2’-5’oligoadenylate which binds and activates RNAseL to destroy both viral and host RNA, shutting down virus replication and host protein expression. Both pathways induce apoptosis
52
IFN pathway
53
Dana Philpott
showed NOD1 and NOD2 proteins recognize bacterial peptidoglycans.
54
Gabriel Nunez
showed NALP3 recognizes peptidoglycans
55
NOD Like receptors
similar to TLR and RLR proteins, NOD Like Receptors (RLR) have crescent shaped α-helical domains to bind ligands. NLR can bind a wide variety of host and microbial ligands, as well as sense changes in intracellular ions, and induce apoptosis, inflammatory cytokines, or cellular differentiation humans have 22 known RLR, mice have 33 28
56
NLR Signal
Binding of ligands (either microbial or due to cell damage) results in oligomerization of NLR, recruitment of adapter proteins (ASC) and activation of Caspase-1. Caspase-1 converts pro-cytokines into active versions that are secreted from the cell Main cytokines are IL-1β and IL-18 which are potent activators of inflammation (vasodilation, cell recruitment, and innate activation).
57
NLR Signals Result in Caspase-1 Activation
58
TLR and NLR Pathways Intersect
TLR signals increase expression of pro-IL-1β and pro-IL18. NLR signals result in conversion of pro-IL-1β to active IL-1β. Secreted IL-1β binds to IL-1β receptor, further increasing expression of MyD88 and IRAK4 (downstream TLR signaling intermediates). IL-1βR also signals through MyD88/IRAK4
59
TLR and NLR Pathways
60
Review of Innate Recognition of Microbes
61
62

MIC 420 (2 decks)

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