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BDS1 Pathology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

What does humoral mean?

A

Driven by macromolecules e.g. antibodies

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2
Q

What doe cellular mean?

A

Does not involve macromolecules but driven by cells e.g. T cells

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3
Q

What are the five groups of disease causing agents?

A
  • Bacteria
  • Viruses
  • Fungi
  • Protozoa
  • Helminths (worms)
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4
Q

Innate immunity is the first line of defence - how many days does it take to kick in?

A

1-4 days

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5
Q

What is meant by the innate immune system having no-memory or lasting protective immunity?

A

The body doesn’t remember what its innate immune system has been exposed to

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6
Q

When does innate immunity start in the body?

A

It is present from birth

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7
Q

Why is innate immunity seen as being effective?

A

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

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8
Q

What is meant by the responses being non-specific?

A

Responses are broad spectrum - general inflammatory response to pathogens

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9
Q

What does innate immunity recruit to sites of infection?

A

Immune cells

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10
Q

What does the innate immune system rely on to recognise ‘non-self’ cells?

A

Relies on a limited number of germline encoded receptors

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11
Q

How is epithelium a physical barrier to infection?

A

Tightly packed cells creating a physical barrier

Stops microorganisms from invading the tissues - prevent pathogens crossing epithelia and colonising tissues

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12
Q

Name 5 molecules in saliva that protect against microorganisms?

A
  • Antimicrobial peptides
  • Immunoglobins
  • Lactoferrin
  • Lysozyme
  • Cystatins
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13
Q

What are antimicrobial peptides also known as?

A

Host defence peptides

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14
Q

What size are host defence peptides?

A

Small ( less than 50 AA)

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15
Q

What is meant when saying host defence peptides have cationic and amphipathic parts?

A

There are hydrophilic and lipophilic parts

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16
Q

Are high concentrations of host defence peptides required for them to be effective?

A

No, they are effective in low concentrations

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17
Q

What do host defence peptides do to membranes?

A

Attach and disrupt membranes - can crack open membranes (specificity for microbial over host)

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18
Q

What are the 4 major families of host defence peptides?

A
  • Beta-defensins
  • Human neutrophil peptides
  • Cathelicidins
  • Psoriasin proteins
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19
Q

What does cationic mean?

A

Positively charged

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20
Q

Where is secretory IgA found?

A
  • Produced at mucosal surfaces

- Unlike most other antibodies does not require interaction between B and T cells

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21
Q

How does IgA work?

A
  • Binds to antigens
  • Binds to flagella and can prevent motility
  • Binds to and neutralises bacterial toxins
  • Cross links target macromolecules and bacteria therefore trapping them and preventing effects on the mucosa
  • Prevents attachment of bacteria to mucosal surfaces
  • Directly by binding to specific adhesion molecules
  • Indirectly due to negative charge and hydrophilic AA creating a ‘hydrophilic shell’
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22
Q

How does the body recognise danger?

A

By the use of an array of receptors - pattern recognition receptors
These are present on a variety of cells: immune cells and epithelial cells

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23
Q

Which receptors are activated by bacteria?

A
  • Toll-like receptors
  • NOD-like receptors
  • Scavenger receptors
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24
Q

Which receptors are activated by viruses?

A
  • Toll-like receptors
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25
Q

Which receptors are activated by fungal pathogens?

A
  • Dectin and glucan receptors
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26
Q

What effects can the activation of receptors by microorganisms cause?

A
  • Activate expression of genes that promote innate immune responses
  • Aid internalisation of bacteria
  • Promote phagocytosis of bacteria
  • Promote activation of immune cells
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27
Q

What are toll-like receptors?

A

Pattern recognition receptors

- 10 identified in humans

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28
Q

Why are toll-like receptors successful?

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 readily be modified

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29
Q

What are Microbial (pathogen) associated molecular patterns (M(P)AMP’s) by toll like receptors?

A

Prevents microorganisms from evolving as if they try to modify themselves they are killed

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30
Q

What are different toll-like receptors activated by?

A

Different microorganisms

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31
Q

Name different antigens present on microorganisms?

A
  • Lipoteichoic acid (LTA)
  • Lipopolysaccharide (LPS)
  • Lipoproteins (LP)
  • Glycophosphatidylinositol (GPI)
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32
Q

Which toll-like receptors are found inside the cell?

A

3,7 and 9

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33
Q

What do we think are the functions of the 10 TLR found in humans?

A
  • Evidence for role in viral infection

- Evidence as an ‘anti-inflammatory’ TLR

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34
Q

Which cells express pattern recognition receptors?

A
  • Epithelial cells (keratinocytes/fibroblasts)

- All immune cells

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35
Q

What does signalling of PRR’s and activating immune cells cause them to directly do?

A

Promote cell functions e.g. phagocytosis

36
Q

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

A
  • Cytokines
  • Interferons (response to viruses)
  • Chemokines
  • Antimicrobial peptides (production of these is ramped up)
  • Other enzymes and inflammatory mediators
37
Q

What are cytokines?

A

Small proteins that are signalling molecules to co-ordinate immune responses

38
Q

Cytokines are grouped into families by structure. What are the 3 main families of cytokines?

A
  • Interleukin-1 family (e.g. IL-1alpha, IL-1beta)
  • TNF family (e.g. TNF alpha)
  • Interferons
39
Q

What does autocrine mean?

A

Alter the behaviour of a cell from which they were secreted (can be released from cell but also acts upon cell)

40
Q

What does paracrine mean?

A

Alter the behaviour of neighbouring cells (can be released and act upon neighbouring cells)

41
Q

What does endocrine mean?

A

Enter circulation and alter behaviour of distant cells (cell can be released and act upon cells throughout the body)

42
Q

What are the consequences of cytokine signalling? (what does the signalling of cytokines induce?)

A
  • Cytokines and chemokines - shapes type of immune response
  • Antimicrobials - Invading organisms
  • Growth factors - Tissue remodelling and repair
  • Receptors - Differentiation and proliferation
43
Q

What do chemokines do?

A
  • Small signalling proteins - rather than initiating signals these recruit immune cells to target areas in the body
  • Predominantly involved in recruitment of immune cells to site of inflammation
44
Q

Why are chemokines called that?

A

As they set up chemokine gradients

45
Q

What are chemokines also known as?

A

Chemotactic cytokines

46
Q

What are the 4 classes of chemokines?

A
  • C chemokines (2 members)
  • CC chemokines (31 members)
  • CXC chemokines (18 members)
  • CX3C chemokines (1 member)
47
Q

How are chemokines classed into different groups?

A

Depending on the spacing of their first 2 cystine residues

48
Q

How do different types of chemokines recruit different types of immune cells?

A

Different chemokines give out different signals - if they give out the right signal they get the right antibodies recruited

49
Q

What is in charge of dictating and shaping immune responses?

A
  • Cytokines and chemokines
  • The immune system is all about balance - can ramp up response to get rid of threat but needs to know when to switch off
50
Q

How do neutrophils know where to go to get to the site of infection?

A
  • They are attracted along a CXCL8 (IL-8) gradient to site of inflammation
  • They are attracted there by chemical signals that are released by other cells of the immune system or by invading microbes
51
Q

What does diapedesis mean?

A

Pulling through - CD31 helps pull through neutrophils

52
Q

Explain the process of neutrophil migration?

A
  • At sites of injury, infection or inflammation, cytokines are released and stimulate endothelial cells that line adjacent blood vessels
  • The endothelial cells then express surface proteins called selectins
  • Selectins bind to carbohydrates displayed on the membrane pf the neutrophils causing them to stick to the walls of the blood vessels
  • This binding interaction is of sufficiently low affinity that the neutrophils can literally roll along the vessel walls in search for points to enter the vessel
  • There they adhere tightly and squeeze between endothelial cells without disrupting the vessel walls and then crawl out of the blood vessel into adjacent connective tissues
53
Q

What are the 3 main families of adhesion molecules?

A
  • Selectins
  • Integrins
  • Immunoglobin superfamily
54
Q

What do adhesion molecules do?

A

Promote cell-cell interactions

55
Q

What are adhesion molecules important for?

A
  • Immune trafficking

- Also important for interactions between immune cells

56
Q

What is the primary function for neutrophils?

A

To engulf and destroy invading pathogens

57
Q

What is the degranulation function of neutrophils?

A
  • Granules in cell vesicles containing numerous antimicrobial peptides and enzymes
  • released upon activation of TLR’s
  • Neutrophils engulf 1 or 2 bacteria and then die - they only last a few hours
58
Q

What are the neutrophil NETs (neutrophil extracellular traps) function of neutrophils?

A
  • Activation induces neutrophils to release proteins and some genetic material (chromatin) to form extra-cellular fibril matrix
  • Traps pathogens
  • Many antimicrobials also associated with the NET so bacteria ‘held’ whilst ‘administered’
59
Q

What are the activated functions of macrophages?

A
  • Phagocytosis and activation of bactericidal mechanisms

- Antigen presentation

60
Q

What is the process of monocytes being converted into macrophages?

A
  • Monocyte binds to adhesion molecules on vascular endothelium near site of infection and receives chemokine signal
  • The monocyte migrates into the surrounding tissue
  • Monocyte differentiates into a macrophage and migrates to the site of infection
61
Q

What are macrophages defence against microbes?

A
  • Phagocytosis
  • Release of antimicrobials and enzymes
  • Antigen presentation - link to adaptive immunity (long term protection) - where innate immunity stops and active immunity starts
62
Q

After defending against microbes what do macrophages do?

A
  • Clearance of damages tissue and cells; e.g. expended neutrophils
  • Promote healing and repair responses
63
Q

Granules are vesicles. What preformed mediators can they contain?

A
  • Proteinases - enzymes that break down different protein agents
  • Antimicrobials (AMPs, lactoferrin)
  • Chemical mediators
64
Q

What stimuli produce the release of granules?

A
  • M(P)AMPs
  • Compliment proteins
  • Cytokines and other inflammatory mediators
65
Q

What do mast cells produce?

A

Histamine

66
Q

What do anti-histamines do?

A

Blocks the action of histamine, control the unwanted immune response to an antigen

67
Q

Does degranulation play a role in allergy?

A

Yes

68
Q

What are the functions of phagocytes?

A

Phagocytosis:

  • Break down pathogens
  • Removal of tissue
  • Antigen presentation
  • Safely break down and dispose of apoptotic cells
69
Q

Name the 2 types of antigen-presenting cell?

A

Non-professional:
- Epithelial cells/fibroblasts/endothelial cells

Professional:

  • Macrophages
  • Dendritic cells
70
Q

What is the link between innate and adaptive immunity?

A

Antigen presentation

71
Q

Which 2 types of cells are key antigen presenting cells?

A

Monocytes and dendritic cells

72
Q

What 4 enzymatic cascade systems are found in plasma?

A
  • Complement
  • Kinins
  • Coagulation factors
  • Fibrinolytic system
    (these systems are interrelated and produce various inflammatory mediators)
73
Q

How many plasma and cell surface proteins are fond in the compliment system?

A

More than 30

74
Q

What is the function of compliment components in the enzymatic cascade system?

A

Act as a primary defence system against bacterial/viral pathogens (works in conjunction with antibodies - link to adaptive immunity)

75
Q

Where do most plasma compliment proteins come from?

A

Liver hepatocytes but tissue macrophages contribute also to local levels

76
Q

What are many complement proteins termed?

A

Acute phase proteins - any of the plasma proteins whose concentration increases or decreases by at least 25% during inflammation. They help mediate both positive and negative effects of acute and chronic inflammation

77
Q

What are the 3 compliment pathways?

A
  • Classical (antigen-antibody)
  • Alternative (foreign cell surface)
  • Lectin (recognising mannose on pathogen) (mannose is a sugar)
78
Q

What is the compliment classical pathways initiating factor?

A

Antibody attached to microbe

79
Q

What is the compliment alternative pathways initiating factor?

A

Microbial cell wall

80
Q

What is the mannose binding lectin compliment pathways initiating factor?

A

Carbohydrates on pathogen surface

81
Q

What are the compliment pathways innate defence functions?

A
  • Trigger inflammation
  • Attract phagocytes
  • Opsonize antigens (make cell more susceptible to phagocytosis)
  • Cause cell lysis
  • Activate naïve B-lymphocytes
  • Remove immune complexes
82
Q

What are the range of effects anaphylatoxins have on immune responses?

A

Promote immune cell recruitment:

  • neutrophils
  • macrophages

Act on neutrophils:
- Degranulation

Act on macrophages:

  • Promote cytokine expression
  • Promote antigen presentation
  • Promotes degranulation

Act on mast cells:
- Degranulation (histamine release)

Regulate adaptive immune responses:
- T-cells and B-cells

83
Q

Where do the 3 complement pathways converge?

A

At production of C3 convertase

84
Q

What does the downstream formation of membrane attack complex require?

A

Formation of C5 convertase

85
Q

What does MAC do to bacteria?

A

Destroys bacteria by creating membrane pore

BDS1 Pathology (14 decks)

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