innate immunity Flashcards

1
Q

what are the innate immune mechanisms of the oral cavity?

A
  • barrier functions
  • saliva
  • initiation of innate immune responses
  • recognition of threats
  • signalling pathways initiating immune responses
  • cytokines and chemokines
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2
Q

what is innate immunity?

A

first line of nonspecific defence against the oral microbiota
- no lasting memory

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3
Q

what is adaptive immunity?

A

specific and acquired

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4
Q

what is humeral response mediated by?

A

mediated by antibody molecules that are secreted by plasma cells

“liquid” “fluid”
blood
yellow bile
black bile
phlegm

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5
Q

how does immune system respond to infection? 3

A
  • tissue homeostasis is essential
  • commensals (organisms doesn’t cause disease) elicit low level immune response
  • pathogens destroyed in hours and rarely causes disease
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6
Q

when does the innate immune response occur?

A

first line of defence
1-4 days

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7
Q

why is the innate immune response effective?

A

regular contact with potential pathogens which are destroyed within minutes or hours only rarely causing disease

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8
Q

is the innate immune response specific or nonspecific?

A

non specific

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9
Q

does innate immune response allow for protective immunity?

A

no memory or lasting protective immunity

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10
Q

what does the epithelium (physical barrier) do in innate immunity?

A
  • produce antimicrobial peptides
  • produce cytokines and chemokines
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11
Q

what are the innate cell subsets in innate immunity?

A
  • phagocytic cells (macrophages, neutrophils)
  • antigen presenting cells (dendritic cells)
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12
Q

what does the chemokine and cytokines do in innate immunity?

A
  • chemokine = cell recruitment
  • cytokine = cell activation/ proliferation
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13
Q

what is the rile of the physical barrier (epithelium)?

A

epithelial barriers produce a number of different compounds

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14
Q

what compounds do epithelial barriers produce in the oral cavity?

A
  • antimicrobial peptides
  • immunoglobulins (secretory IgA)
  • lactoferrin
  • lysozyme
  • cystatins
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15
Q

what is the function of antimicrobial peptides?

A

to kill microbes (binding to cell wall, attaching to surface and disrupt membrane) and modulate immune system.

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16
Q

name 4 major families of antimicrobial peptides?

A

b - defensins
human neutrophil peptides (HNPs)
cathelicidins
psoriasis proteins

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17
Q

at what concentration are antimicrobial peptides most effective?

A

effective at low concentrations

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18
Q

how does secretory immunoglobulin S (SlgA) form a protective layer?

A

absorbing saliva

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19
Q

what does dimeric form of SlgA allow for?

A

attachment to multiple microbes

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20
Q

what does secretory immunoglobulin A do?

A

binds and neutralises pathogen and toxins externally and internally.

21
Q

what is lactoferrin?

A

glycoprotein that transports iron ions but has antimicrobial activity
- present in saliva
produced by neutrophils

22
Q

what is lysozyme?

A

targets cell wall of bacteria
- present in saliva
- produced by macrophages/ neutrophils

23
Q

what is cystatins?

A

anti-protease activity
supports remineralisation of teeth

24
Q

what does the epithelium do in responding to pathogenic threats?

A

acts as a physical and immunological barrier

25
Q

what protects the epithelium in immune response?

A

salivary components and their broad spectrum antimicrobial activity

26
Q

what receptors do cells involved in immune responses have?

A

receptors for components of microorganisms

27
Q

what are microbial agents?

A

toxins and virulence factors

28
Q

what actives the immune response in microbial regions?

A

receptor activation

29
Q

what are the main receptors?

A

Toll-like receptors

30
Q

what are the other type of receptor for fungi?

A

diction and gluten

31
Q

what are the other type of receptor for bacteria ?

A

NOD-like receptors

32
Q

what are the other type of receptors for microbial and allergen recognition?

A

protease-activated receptors

33
Q

what are the main roles for the other receptors?

A
  • promote phagocytosis of microbes
  • promote activation of immune cells
34
Q

what are PRRs ?

A

Pattern Recognition Receptors

35
Q

what can PRRs recognise?

A

Pathogen Associated Molecular Patterns PAMPs

36
Q

describe the host cell pathogen interaction sequence?

A

bacteria (lipopolysaccharide/lipoteichoic acid)>
TLR4 or TLR2
then
TLR2>
NF-kB (transcription factor)
cytokine/chemokine transcription - nucleus
cytokine/chemokine translation and processing
cytokine/chemokine secretion
then inflammatory response

37
Q

what size are cytokines?

A

small <80kDa

38
Q

what are cytokines?

A

signalling molecules to coordinate immune responses

39
Q

name and describe the 3 functions of cytokines?

A

AUTOCRINE = alter behaviour of cell from which they were secreted eg. self regulating
PARACRINE = alter behaviour of neighbouring cells
ENDOCRINE = entree circulation and alter behaviour of distant cells

40
Q

what do cytokine receptors recognise and what happens?

A

recognise cytokines
induces conformational changes in majority of receptors intracellularly

41
Q

what is the difference between cytokines and chemokines?

A

chemokines = tell immune cells where to go (movement)
cytokines = tell immune cells what to do

42
Q

what are chemokines?

A

small signalling proteins - chemotactic cytokines
= involved in recruitment(directing)

43
Q

what is chemotaxis?

A

movement of a cell in a direction corresponding to a gradient of increasing and decreasing concentration of a particular substance (chemokines)

44
Q

what are the 4 classes of chemokines?
how many members do they each have?

A

C chemokines = 2
CC chemokines = 31
CXC chemokines = 18
CX3C chemokines = 1

45
Q

what produced the chemokines CXCL8?

A

monocytes
macrophages
fibroblasts
epithelial cells
endothelial cells

46
Q

what are the receptors for chemokine CXCL8?

A

CXCR1
CXCR2

47
Q

what does the oral mucosa produce to prevent infection?

A

Anti Microbial Peptides (AMPs)
Secretory IgA
Lactoferrin
Lysozyme
Cystatins

48
Q

how do you initiate inflammatory responses?

A

activation of intracellular signalling pathways which lead to ‘switching on’ of genes