Innate immunity 1 Flashcards

1
Q

What is the host response aimed at?

A

Eradicating the pathogen

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2
Q

What does the protection mechanism of the immune system do?

A

Decides what is host and what is foreign organism
Decides what organisms are commensal and pathogenic
Decides what type of pathogen is causing danger and elicits immune response accordingly

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3
Q

What do many pathogens arise from?

A

A deleterious (to cause harm) immune response

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4
Q

What does the humoral component of the immune response involve?

A

Macromolecules, e.g., antibodies

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5
Q

What is the time frame of immediate innate immunity?

A

0-4 hours

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6
Q

What are the stages of immediate innate immunity?

A

Infection
Recognition by performed, non specific and broadly specific effectors
Removal of infectious agent

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7
Q

What is the time frame of early induced innate response?

A

4-96 hours

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8
Q

What are the stages of early induced innate response?

A

Infection
Recruitment of effector cells
Recognition of PAMPS (pathogen associated molecular patterns)
Removal of infectious agent

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9
Q

What is the time frame of the adaptive immune response?

A

More than 96 hours

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10
Q

What are the stages of the adaptive immune response?

A
Infection 
Transport of antigen to lymphoid organs 
Recognition by naive B and T cells 
Clonal expansion and differentiation to effector cells 
Removal of infectious agent
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11
Q

What sort of immune response do commensals elicit?

A

Low level- if any

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12
Q

What are the 5 groups of disease causing agent?

A
Bacteria 
Viruses 
Fungi
Protozoa 
Helminths
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13
Q

What do disease symptoms depend on?

A

Where the pathogen replicates and the damage it causes

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14
Q

What do epithelial/endothelial cells and fibroblasts contribute to?

A

Innate immune response

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15
Q

What is innate immunity involved in?

A

The recruitment of immune cells to sites of infection

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16
Q

What does innate immunity rely on?

A

A limited number of gremlin encoded receptors to recognise ‘non self’

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17
Q

What sort of protection is epithelium?

A

An intrinsic, physical barrier

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18
Q

How are epithelial cells arranged?

A

Tightly packed cells joined by tight junctions

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19
Q

What prevents attachments of microorgnisms to epithelium?

A

Airflow.
In skin and gut, longitudinal flow of air
In lungs, movement of mucous by cilia

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20
Q

How do epithelial cells in various locations offer chemical protection?

A

Fatty acids in skin
Gut- low pH for pepsin
Skin, gut, lungs- antibacterial peptides
Eyes, nose- salivary enzymes (LYSOZYME)

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21
Q

What antimicrobials does saliva contain?

A

Lactoferrin
Lysozyme
Antimicrobial peptides
Immunoglobins (secretory IgA)

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22
Q

What does lactoferrin do?

A

Lactoferrin transfers iron to cells and controls levels of iron in blood and secretions. Bacteria need iron but lactoferrin removes it from them

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23
Q

How does lactoferrin effect bacterial pathogens?

A

It binds to the bacterial lipopolysaccharide and destabilises the bacterial membrane. It therefore disrupts the bilayer and creates osmotic stress.

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24
Q

How does lysozyme effect bacteria?

A

It cleaves the peptidoglycan, so breaks bacteria cell wall

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25
Q

Where is lysozyme found?

A

In tears, saliva, nasal secretions

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26
Q

What happens when lactoferrin and lysozyme work together?

A

It gives lysozyme better access to peptidoglycan layer

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27
Q

What size are antimicrobial peptides?

A

Very small

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28
Q

What parts do antimicrobial peptides have?

A

They are cationic and amphipathic , which means they have hydrophillic and lipophillic parts

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29
Q

What do antimicrobial peptides form?

A

They form pores, so can attach and disrupt membranes

30
Q

At what concentration are antimicrobial peptides most effective?

A

In low concentrations

31
Q

What are the major antimicrobial peptides found in the mouth?

A

B- defensins
Numan neutrophil peptides (HNP)
Cathelicidins
Psoriosin proteins (S100 family)

32
Q

What is IgA?

A

An antibody but has a different role to normal antibodies as it does not require interaction between T and B cells

33
Q

Where is IgA produced and found in high levels?

A

It is produced at mucosal surfaces, and is found in high levels in secretions

34
Q

What can IgA bind to?

A

To antigens
To flagella to prevent motility
To bacterial toxins to neutralise them

35
Q

What do cross links of IgA target and what does this do?

A

Targets macromolecules and bacteria, therefore trapping them and preventing effects on mucosa

36
Q

How does IgA prevent attachment of bacteria to mucosal surfaces?

A

Directly- by binding to specific adhesion molecules

Indirectly- due to negative charge and hydrophillic amino acids creating a ‘hydrophillic shell’

37
Q

Where is secretory IgA produced?

A

At mucosal surfaces

38
Q

What does the interaction between microbes and receptors initiate?

A

Innate immune responses

39
Q

What are the receptors called and where are they present?

A

They are called pattern recognition receptors (PRR’s) and are present on immune cells and epithelial cells

40
Q

What receptors (PRR’s) can bacteria bind with?

A

Toll-like receptors (TLR’s)
NOD-like receptors
fMLP
Scavenger receptors

41
Q

What receptors (PRR’s) do viruses bind with?

A

Toll-like receptors (TLR’s)

42
Q

What receptors (PRR’s) do fungal pathogens bind with?

A

Dectin and glucan receptors

43
Q

What can interactions between microbes and receptors (PRR’s) do?

A

Activate the expression of genes that promote innate immune responses
Aid internalisation of bacteria
Promote phagocytosis of bacteria
Promote activation of immune cells

44
Q

How many toll-like receptors have been identified in humans?

A

TCR’s are PRR’s, 10 identified in humans

45
Q

How do toll-like receptors work?

A

They recognise constituents of microbial cell walls or pathogen-specific nucleic acids that are essential to the integrity, function or replication of microbes/viruses that cannot be readily modified

46
Q

What are PAMP’s??

A

Pathogen associated molecular patterns (PAMP’s) are molecules associated with pathogens. PAMP’s bind to, and are recognised by toll-like receptors and pattern recognition receptors

47
Q

What do PAMP’s activate?

A

PAMP’s activate innate immune responses by identifying some conserved non-self molecules. They contain features that body cells don’t have, such as lipopolysaccharide

48
Q

Which TLR’s are found within the cell?

A

3,7 and 9

49
Q

What does virus activation of TLR’s induce?

A

Can induce changes in gene expression, translation and transcription, which can activate molecules such as protein kinases

50
Q

What are c-type lectin receptors essential for?

A

Anti-fungal immunity

51
Q

What do c-type lectin receptors recognise?

A

Carbohydrates in fungal cell wall

52
Q

What are the c-type lectin receptors?

A

Dectin 1&2
Mannose receptor
DG-SIGN
Mincle

53
Q

What does activation of CLR’s (c-type lectin receptors) induce?

A

Changes in gene expression

54
Q

What cells express PRR’s??

A
Epithelial cells (keratinocytes/fibroblasts)
All immune cells
55
Q

What does signalling of PRR’s activate?

A

Activates immune cells directly, promotes functions e.g., phagocytosis

56
Q

What does signalling of PRR’s induce cells to express?

A

Cytokines
Interferones
Chemokines
Antimicrobial peptides

57
Q

What are cytokines?

A

Small proteins, signalling molecules which coordinate immune responses

58
Q

In what manner can cytokines act?

A

Autocrine- alter behaviour of cell from which they are secreted
Paracrine- alter behaviour of neighbouring cells
Endocrine- enter circulation and alter behaviour of distant cells

59
Q

What are interferons?

A

A type of cytokine, important in anti-viral immunity

60
Q

What do interferons do?

A

They stop viral replication, and promote immune response against virus infected cells

61
Q

How do interferons stop viral infection?

A

They switch on expression of proteins in cells which inhibit replication

62
Q

How do interferons promote immune response against virus infected cells?

A
They activate NK cells to kill the virus infected cells
They increase synthesis and surface expression of MHC class 1, which targets infected cells for destruction by CD8 cytotoxic T cells
63
Q

What are chemokines?

A

Small signalling proteins, chemotactic cytokines

64
Q

Why are chemokines produced?

A

Due to TLR and NF-kB activation

65
Q

What do chemokines do?

A

Mainly involved in recruitment of immune cells to site of inflammation

66
Q

How are chemokines grouped?

A

Grouped into 4 classes, depending on spacing of their first 2 cysteine residues

67
Q

What is the concentration of chemokines like?

A

In highest conc. towards threat. Immune cells follow the trail of the chemokine gradient

68
Q

What are the 4 classes of chemokine and how many members does each have?

A

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

69
Q

What do cytokines and chemokines dictate?

A

They dictate and shape immune response

70
Q

How is the immune system balanced?

A

When there is threat- pro inflammatory molecules are produced
When threat is cleared- anti inflammatory molecules are produced to reduce the immune response