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Immunology > 49-Barriers and Pathogen Recognition > Flashcards

49-Barriers and Pathogen Recognition Flashcards

1
Q

physical barrier of skin

A

multiple layers with tight junctions

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2
Q

mechanical barrier of skin

A

shedding every 28 days and perspiration

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3
Q

chemical barrier of skin

A

dry, cool, salty, acidic pH 5, lysozyme to degrade peptidoglycan, sebum

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4
Q

physical barrier of mucous membrane

A

goblet cells creating slime layer, epiglottis blocking respiratory tract

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5
Q

mechanical barrier of mucous membrane

A

cilia in lower respiratory

tears, blinking, urination, defecation, sneezing, coughing, vomiting

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6
Q

chemical barrier of mucous membrane

A

low pH in stomach and vagina, release of antibodies, lysozyme in tears and saliva

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7
Q

what is normal microbial flora

A

commensal bacteria found all over body, different species at each site of colonization

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8
Q

how does normal flora inhibit pathogens

A

compete for nutrients, compete for space, produce toxins, alter growing conditions

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9
Q

how do barriers fail

A

wounds, defective barrier, chronic disease, malnutrition, insect bite, pathogenicity

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10
Q

what happens when barriers fail

A

innate immune response starts quickly

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11
Q

what does it mean that the innate is constitutive

A

does not change over your life

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12
Q

what does it mean that the innate is conserved

A

responds to conserved features of pathogens like cell wall, peptidoglycan

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13
Q

what are the goals of the innate response?

A

detect and kill pathogen, sound alarm to bring in more cells, activate the adaptive response

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14
Q

what are pattern recognition receptors

A

recognize infection in coming by recognizing pathogens

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15
Q

what are the types of pattern recognition receptors

A 
Toll like (TLR)
Nod like (NLR)
RIG-I
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16
Q

what do TLR recognize

A

PAMPs-conserved features of pathogens essential for viability
DAMPs- human derived signals which start inflammation

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17
Q

what are Pathogen Associated Molecular Patterns

A

PAMPs, conserved features of pathogens essential for viability

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18
Q

What are Danger Associated Molecular Patterns

A

DAMPs, human derived signals, drive non infectious inflammation and start inflammation caused by infection

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19
Q

Where are TLRs found

A

cell surface and intracellularly (phagolysosome or endosome)

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20
Q

what do cell surface TLRs recognize

A

bacterial and fungal cell wall

21
Q

what do intracellular TLRs recognize

A

nucleic acid

22
Q

what happens with inappropriate TLR activation

A

chronic inflammation and human disease

23
Q

what activates TLR

A

dimerization with leucine ligands

intracellular region has Toll/IL-1 (TIR) domain

24
Q

what drives intracellular signaling of TLR

A

dimerization if TIR domain

all TLR except TLR3 interact with MyD88 drive activation of NF-kB for inflammation

25
Q

what do TLR4 and TLR3 bind to

A

TRIF to activate NF-kB and IRF3 to produce type 1 interferons for antiviral

26
Q

where are NLR found

A

cytoplasm of multicellular eukaryotes

27
Q

what facilitates oligomerization of NLR

A

NACHT domain

28
Q

what facilitates ligand sensing and regulate NLR

A

leucine rich repeats

29
Q

what drives intracellular signaling of NLR

A

N terminal domain

30
Q

what activates NLR

A

many things: bacterial, viral, fungal, ion efflux, ATP, human protiens

31
Q

Explain how NLRs drive expression of inflammatory cytokine

A

1-oligomerization of NLR using NLR ligand
2- recruitment of intracellular signaling molecules to activate NF-kB and MAP
3-NF-kB and MAP induce inflammation and chemokines

32
Q

altered activation of NLR leads to what

A

autoimmune disease
1- Loss of function-prevent NF-kB activation, Crohn’s disease
2-gain of function- constitutive NF-kB activation, autoinflammatory

33
Q

what induces inflammasome

A

NLRP1, 3, 4, 6

34
Q

how do NLRs induce inflammasome

A

1-priming induces production of pro IL-1B and pro IL-18
2-presence of ROS, PAMP, DAMP, ion efflux result in the formation of inflammasome
3-inflammasome (caspase 1) cleaves to IL-1B and IL-18

35
Q

what activates NLRP3

A

potassium efflux, ROS, phagolysosomal release

36
Q

polymorphisms in inflammasome lead to what

A

autoimmunity, gain of function and chronic inflammation

37
Q

what has anakinra been approved for

A

RA as a IL-1 receptor antagonist

38
Q

how do pathogens influence inflammasome

A

inhibit it to enhance pathogenesis

39
Q

what are the RIG-I family members

A

RIG-I, MDA5, and LGP2

40
Q

what does the helicase domain/DExD/H do in RIG-I family

A

bind viral RNA ligand

41
Q

what does the regulatory domain in RIG-I family do

A

control receptor funciton

42
Q

what does the CARD domain do in the RIG-I family

A

intracellular signaling in RIG-I and MDA5

regulates RIG-I and MDA5 in LGP2

43
Q

RIG-I binds to what

A

short viral RNA on terminal 5’ triphosphate

44
Q

MDA5 binds to what

A

large RNA molecules internally and results in oligomerization

45
Q

what activates the CARD domains

A

binding of viral RNA to RIG-I or MDA5

46
Q

activated RIG-I and MDA do what

A

bind to adaptor protein IPS-1 (found on mitochondria)

47
Q

activation of IPS-1 does what

A

NF-kB and IRF3 activation to produce interferons and antiviral

48
Q

how do viruses suppress function of RIG-I and what does it lead to

A

inhibit RIG-I signaling

chronic viral infections

Immunology (19 decks)

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