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principles of infectious diseases > innate and adaptive immune system > Flashcards

innate and adaptive immune system Flashcards

1
Q

innate system

A

evolutionary origin - earliest animals - all invertebrate and vertebrates

principal cells - phagocytes, natural killer cells

principal molecules - complement, acute phase proteins, cytokines

specificity of recognition - broad

speed of action - rapid

development of memory - no

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2
Q

adaptive system components

A

evolutionary origin - vertebrates only

principal cells - lymphocytes

principal molecules - antibody, cytokines

specificity of recognition - highly specific

speed of action - slow

development of memory - yes

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3
Q

innate vs adaptive

A

the innate system is a system that is always available, whereas the Adaptive you has to have encountered a pathogen for that system to develop

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4
Q

non specific defence system/ innate immunity - professional phagocytes

A

ingest and kill microbes (neutrophils, monocytes, macrophages, mast cells and dendritic cells)

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5
Q

non specific defence system/ innate immunity - complement

A

set of proteins produced by liver which mediate protection against some microbes

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6
Q

non specific defence system/ innate immunity - NK cells

A

important for protection against viruses
- attack and kill infected host cells (release perforins and granzymes which induce apoptosis)
- release the cytokine IFN gamma which protects adjacent cells from infection

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7
Q

non specific defence system/ innate immunity - dendritic cells

A

link between innate and adaptive immunity
- they present antigens to T cells to help direct adaptive immunity
- closely related to macrophages

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8
Q

non specific defence system/ innate immunity - mast cells and basophils

A

important in acute inflammatory response
- release granules (contain histamine) that result in vasodilation

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9
Q

non specific defence system/ innate immunity - acute phase proteins

A

group of proteins in the plasma
- mainly produced in response to alarm mediators such as cytokines released as a result of infection or tissue
- antimicrobial activity: includes maximising activation of the complement system and opsonising organisms for phagocytosis

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10
Q

non specific defence system/ innate immunity - cytokines

A

small molecules that signal between cells
- includes chemokine: smaller proteins that attract immune cells to infection sites
- often cause symptoms of infection, such as fever, muscle pain and fever like

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11
Q

phagocytes

A

white blood cells and tissue-dwelling cells able to ingest and kill particles:
- macrophages:
- different into tissue macrophages
- derived from monocytes in blood
- neutrophils/ polymorphonuclear cells in blood
- Get moved to tissues in response to a stimulus of infection or injury

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12
Q

phagocytes: neutrophils

A
  • 70% neutrophils
  • 1st to arrive at the site of infection
  • a reserve of 3x10^12 in bone marrow
  • non-dividing, short-lived < 1 day
  • multi-lobed nuclei
  • glycogen storage/ few mitochondria
  • granules - chemical attack - Contain antimicrobial peptides, enzymes, chemicals
  • 10^11 disappear from circulation each day
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13
Q

how do macrophages move to the site of infection

A

Diapedesis
- in response to a signal of infection or tissue injury the early cytokines, tnf alpha, interferon-gamma and interleukin-1 stimulate the expression of selectins and blood vessel endothelia.
- this means that the neutrophils that are in there start to bind to these selectins and it causes them to slow down
- start to stick to the endothelial wall

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14
Q

diapedesis - what happens after the neutrophils bind to selectins

A
  • Then interleukin 8 which gets released by macrophages causes the neutrophils to express integrins on their surface and this causes tighter binding to the endothelia and they bind to ICAMS and VCAMs on the endothelial
    ○ So this is intercellular adhesion molecules or vascular cellular adhesion molecules
    • they bind more tightly and this starts to cause margination
      ○ This is when they flatten against the endothelial wall.
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15
Q

diapedesis - what happens after margination

A
  • Then the blood vessels dilate and this is partly due to platelet activating factor and those vessels become a bit leaky
  • and then the neutrophils are able to squeeze their way between the endothelial cells and they move into tissue
  • then they follow the signal - so they move chemotactically towards the signal Of the infections.
  • They move towards that site and at the same time they’re killing potential starts to be activated.
    This whole process is called diapedesis
  • at the same time as the cells moving out, other factors will also come out of the bloodstream and the endothelial becomes quite leaky.
  • So you get this movement of fluid and Cells and protein factors out of the blood so all of this contributes to inflammation,
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16
Q

diapedesis - inflammation

A

you start to get a bit of swelling because you’ve got fluid build up at the site of the infection and this can cause reddening because you’ve got increased blood flow and you get pain at the site of infection because that pressure of the fluid buildup is pressing on nerve endings

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17
Q

macrophages

A

Macrophages are synthesised in the bone marrow and they go into the blood
- when they’re in the blood they are monocytes and then the monocyte differentiate into macrophages as they leave the blood and enter issues.
- So macrophages tend to be found in the more vulnerable parts of the body - present in tissues and Patrol those areas and protect from infection
- in response to signals of infection, you’ll get more monocytes being pulled out of the blood to that site of infection and they differentiate into macrophages,
- slower than the neutrophil response
- longer living

18
Q

how do phagocytes recognise microbes

A

this is part of the innate immune system.
-they’re recognizing highly conserved structures on microbes and they do this using pattern recognition receptors that recognise pathogen associated molecular patterns (PAMPs) and also DAMPs

19
Q

what are PAMPs

A

PAMPs are small molecular motifs that are conserved within whole classes of microbes and not present in the host
- Usually they are essential for survival
- Pathogens can easily get rid of them
- They show minimal variation

20
Q

toll like receptors

A

Toll like receptors are a subgroup of receptors that are important in causing signalling events in the phagocyte that then control the downstream immune events

21
Q

what do toll like receptors do

A

Toll like receptors recognize microbial components and they do this in association with the other receptors.
-The toll-like receptors are able to Signal the presence of a pathogen and then they trigger the expression of co-stimulatory molecules and direct the immune system in the right way,
- they’re important for Activation of macrophages And development of adaptive immunity.

22
Q

TLR-4

A

best characterised toll-like receptor
- a transmembrane protein that acts with CD14 to generate a transmembrane signal -> cytokine release

23
Q

toll like receptor action

A

what happens is you’ve got a gram-negative bacteria cell that’s got LPS in the outer membrane.
- If the bacteria get lysed or they shed the LPS it gets Bound by the LPS binding protein and taken to the cd14 receptor on the surface.
- Then that interacts with the toll like receptor.
- And then there’s a couple of accessory proteins that are important.
- But basically what happens is this interaction causes appropriate signaling events,

24
Q

diversity of TLRs

A

there’s the diversity of these toll-like receptors that recognize different pamps.
- So it means that these phagocytes can direct the immune system accordingly based on which pamps are being detected.

  • The toll-like receptors can either function as homodimers or heterodimers,
  • and some of them work in combination.
    These are heterodimers and that can alter their specificity slightly
25
Q

how do phagocytes kill microbes

A

receptors on the phagocyte surface recognize the pathogen
- you start to get pseudopodia forming around the microbe and the phagosome forms, which is a compartment that the bacteria or microbe is in.
- Then that phagosome starts to mature and you get Fusion of lysosomes or granules with that phagosome and that forms a phagolysosome
-The lysosomes contain all the antimicrobial peptides and enzyme - so fuses with the phagosome and then you start to get damage and digestion of the microbe and then you get release of microbial products.

26
Q

antimicrobial mechanisms in phagocytic vacuoles

A

antimicrobial proteins and peptides stored in lysosomal granules
- fuse with the pathogen containing phagosome -> phagolysosome formed

neutrophils possess a variety of enzyme-containing granules
- primary azurophilic granules
- secondary specific granules
- tertiary lysosomal granules

27
Q

lactoferrin

A

Lactoferrin - tightly bind to iron - prevent microbes acquiring iron vitamin B12 binding protein

28
Q

what activates lysosymal enzymes

A

AS THE PHAGOSOME DEVELOPS THE pH in the phagosome drops due to a proton pump added to the membrane of the pump - pumps protons in and reduces the pH
- Causes the activation of all of these acid hydrolases

29
Q

Nramp1

A

pumps metal ions across phagosomal membrane

30
Q

respiratory burst oxidases

A

Produces reactive oxygen species in the phagosome

31
Q

oxygen independent antimicrobial mechanisms

A

low pH - bactericidal or bacteriostatic

hCAP-18, defensins, NSPs, acid hydrolases, BPI, proteolytic enzymes:
- damage to microbial membranes/ bacteriocidal
- degrade dead microbes

B12 binding protein, lactoferrin, Nramp1, calprotectin, lipocalin:
- competition for nutrients/ alter ion availability/ bacteriostatic

lysosome:
- disrupts peptidoglycan/ bacteriocidal

32
Q

neutrophil extracellular traps

A

neutrophils release them
- web of extracellular fibres: DNA, histones, antimicrobial proteins
- activated by a range of mediators: IL-8; LPS

33
Q

what do neutrophil extracellular traps do

A

can kill extracellular pathogens
- high local concentration of antimicrobial components
- limits host damage: stops proteases from diffusing to nearby host tissues
- serve as a physical barrier that prevents further spread of the pathogens

34
Q

macrophage function

A

In the presence of interferon gamma, which gets released from the T cells and TNF alpha which gets released from infected macrophages - this causes macrophage activation
- Causes increased killing action - synthesis of nitric oxide

35
Q

PMNs

A

site of production: bone marrow
operation in marrow: 14 days
duration in blood: 7-10 hours
average life span: 4 days
numbers in blood: 2.5 x10^9
marrow reserve: 10x blood
numbers in tissue: transient

36
Q

macrophages

A

site of production: bone marrow, tissues
operation in marrow: 54 days
duration in blood: 20-40 hours
average life span: months to years
numbers in blood: 0.5 x10^9
marrow reserve: none
numbers in tissue: 100x blood

37
Q

PMNs principle killing mechanisms

A
  • degradative enzymes
  • cationic peptides/ defensins
  • lactoferrin, B12- Binding protein
  • respiratory burst oxidase
  • Nramp1
  • myeloperoxidase
  • calprotectin
  • NETs
38
Q

macrophage principle killing mechanisms

A
  • degradative enzymes
  • cationic peptides/ defensins
  • lactoferrin, B12- Binding protein
  • respiratory burst oxidase
  • Nramp1
  • no myeloperoxidase
  • no calprotectin
  • Nitric oxide
39
Q

PMN major secretory protein

A

lysosyme

40
Q

macrophage Major secretory protein

A

lysosyme, cytokines and NO

principles of infectious diseases (19 decks)

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