Innate immunology Flashcards

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1
Q

Immunity is split into two types of responses

A

Innate and Adaptative

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2
Q

Define immunology

A

the way in which your body defends itself from the outside

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3
Q

Specificity innate immunity

A
  • Present from birth
  • Relatively non-specific
  • No memory
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4
Q

Specificity adaptive immunity

A
  • Involves very specific recognition of precipitating agent (antigen)
  • Powerful memory generated
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5
Q

Primary lymphoid tissues function

A

Produce cells involved in the immune response and educate adaptive immune cells not to recognise ‘self’

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6
Q

Secondary lymphoid tissues function

A

Designed to allow adaptive immune cells and antigens to get together to initiate the adaptive immune response

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7
Q

the innate and adaptive immune system is referred to a ‘smart’ system explain

A

its memory allows it to respond rapidly to a second encounter with a pathogen

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8
Q

dendritic cells are?

A

crucial cells for linking innate and adaptive response

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9
Q

Myeloid progenitor is respinsible for?

A

all/ most cells involved in immunity

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10
Q

Lymphoid progenitor define

A

the precursor for the cells involved in the adaptive immune response. Mainly B & T lymphocytes; there also some natural killer cells

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11
Q

innate immunity stems from?

A

tissue damage from trauma or infection causes complex series of cellular and chemical events which aim to unit spread, to eliminate pathogen/toxins to repair damage

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12
Q

4 types of defensive barries

A

anatomical
physiological
phagocytic
Inflammatory

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13
Q

How does skin act as a defensive barrier?

A

Mechanical barrier that stops the entry of microbes

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14
Q

List anatomical barriers

A

skin
mucosal surfaces

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15
Q

How does mucosal surfaces act as a defensive barrier?

A

Competition for attachment and nutrients
mucus entrapment
cilia propulsion

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16
Q

List physiological defensive barriers

A

Temperature
low pH
Chemical mediators

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17
Q

List examples of chemical mediators involved in defensive barriers

A

lysosomes, interferon, collectins, cytokines and complement proteins

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18
Q

Phagocytic defense barriers involves?

A

specialised white blood cells taking up and destroy pathogens

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19
Q

Endocytosis define

A

Uptake of extracellular material

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20
Q

Phagocytosis define

A

active uptake of particulate material through formulation of finger-like projections of cytoplasm ( & attempted) degradation of material

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21
Q

pinocytosis define

A

uptake of soluble material

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22
Q

How does an inflammatory response act as a defensive barrier?

A

release of many mediators, changes in vascular permeability, serum proteins with anti-bacterial activity

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23
Q

How do phagocytes destroy organism by intracellular mechansims? begin from site of infection

A
  • At site of infection, specialised wbcs take up organisms/toxins
  • Later on in immune responses/in blood other wbcs phagocytose
  • Organism destroyed by intracellular mechanisms
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24
Q

How do phagocytes recognise pathogens?

A

by cell surface receptors that identify the agent as foreign

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25
Q

PAMPS

A

Pathogen Associated Molecular Patterns

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26
Q

PRR

A

Pattern Recognition Receptors

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27
Q

How do phagocytes recognise pathogens directly?

A

PRR bind to molecules,
PAMPs only found on microbes or modified host cells

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28
Q

How do phagocytes recognise pathogens indirectly?

A

Serum proteins (antibodies, complement, lectins) can coat or ‘opsonise’ particles which are then recognised by receptors on phagocytes

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29
Q

destructive enzymes work best at what pH? low or high

A

low pH

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30
Q

Digestion- attempted destruction of taken up material can happen how? 2 ways

A

oxygen independent
oxygen dependent

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31
Q

3 ways digestion can be oxygen independent

A

acidification
enzymes
defensins

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32
Q

acidification (how)

A

phagolysosome acidifies due to lactic acid and H+ produced

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33
Q

enzymes involved in disgestion (oxygen independent)

A

lysosomes, lipases, proteinases

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34
Q

digestion by defensins involves polypeptides. EXPLAIN

A
  • electrostatically attracted to pathogens
  • from pores in the surface
  • most abundant protein in neutrophil granules
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35
Q

Digestion can be attempted by oxygen dependent pathway how?

A

respiratory bust through reactive oxygen or nitrogen intermediates (ROIs & RNIs) also known as free radicals

36
Q

Mechanism for respiratory bust

A

involves cytoplasmic and membrane associated enzymes which oxidise molecules and leave them with unpaired electrons (very unstable)
ROIs & RNIs hvae potent anti-microbial properties that can be secreted by the phagocytes

37
Q

free radicals have potent anti-microbial properties such as:

A

damage proteins, lipids, cell membranes, DNA

38
Q

Summary of phagocytosis

A
  1. Bacterium becomes attached to membrane evaginations called pseudopodia
  2. Bacterium is ingested, forming phagosome
  3. Phagosome fuses with lysosome
  4. Lysosomal enzymes digest captured material
  5. Digestion products are released from cell
39
Q

when bacteria is ingested it forms?

A

a phagosome

40
Q

Membrane evanginations are called?

A

pseudopodia

41
Q

rubor

A

redness

42
Q

calor

A

heat

43
Q

dolor

A

pain

44
Q

tumor

A

swelling

45
Q

Inflammation is one of the body’s early defence reaction to ?

A

infection/ damage

46
Q

5 signs of inflammation

A

Rubor, Calor, Dolor, Tumor, Loss of function

47
Q

Inflammation involves large number of chemicals and cells acting in concert to do what? and why?

A

to increase blood flow, permeability vasculature
why? to limit infection spread and tissue damage, promoting healing

48
Q

permeability vasculature refers to?

A

allowing cells out of the blood into the tissue

48
Q

permeability vasculature refers to?

A

allowing cells out of the blood into the tissue

49
Q

During inflammation how are immune cells activated?

A

At site mediators are released from activated tissue wbcs:
- Stimulate release of granulocytes and monocytes, activate hypothalamus and liver- Acute Phase Protein Production (CRP,SAA,MBL)
- Increase expression of Adhesion molecules on endothelial cells lining blood vessels & on local wbcs
- other factors affect vascular tone and integrity of endothelial layer

50
Q

Where are granulocytes and monocytes released from when stimulated during inflammation?

A

bone marrow

51
Q

when hypothalamus is activated during inflammation, what does this lead to?

A

fever

52
Q

when liver is activated during inflammation what is produced?

A

Acute Phase Protein production ( CRP, SAA, MBL), which bind to a number of “molecules” and oxidise

53
Q

benefit of increasing expression of adhesion molecules during inflammation

A

allows cells to attach to endothelium

54
Q

During inflammation other factors affect vascular tone and integrity of endothelial layer allowing?

A

attached cells to pass into tissues

55
Q

List some inflammatory mediators

A

includes wide range of proteins, lipids and chemicals
-cytokines/chemokines
-enzymatic cascades
-complement components
-prostaglandins and leukotrienes

56
Q

cytokines are categorised how?

A

Pro- inflammatory and anti-inflammatory

57
Q

List of pro-inflammatory

A

IL-1,6, 12, TNF (tumour necrosis factor alpha) IFN (interferon gamma)

58
Q

Fucntion of IL-12

A

Activates adaptive immune responses ( T cells)

59
Q

IFN gamma function

A

acts later on contributing to chronic inflammation by recruiting macrophages to sites of damage/ infection

60
Q

IL-1, IL-6 & TNF alpha are early alarm signals causing local & systemic activation of:

A

fever, vascular permeability, production of acute phase protein increased adhesion of molecule expression

61
Q

what activates T cells in adaptive immunity?

A

IL- 12

62
Q

what IL recruits macrophages to sites of damage/ infection?

A

IFN

63
Q

List cytokines in anti-inflammatory response

A

IL-10

64
Q

chemokines consist of 2 families ,name them

A

CC & CXC

65
Q

Chemotaxis

A

ability of the cell to move up a chemokine gradient

66
Q

on binding specific receptors on wbcs, what do chemokines do?

A

stimulate migration & activation of these cells towards the gradient of the chemokine

67
Q

chemokines are defined by?

A

presence of 4 cysteine residues and sequence of amino acids involving the first two major families

68
Q

fugitaxis

A

works other way of chemotaxis - high to low chemokine gradient
e.g. IL-8

69
Q

fibrinolytic pathway

A

-Endothelial damage
- Activation of Hageman factor (factor XII)
- Activated fibrinolytic system
- Plasmin
- complement activation

70
Q

Plasmin can lead to two different pathways:

A

fibrinolytic and clotting

71
Q

Clotting pathway

A
  • endothelial damage
  • Activation Hageman factor
  • Activated clotting cascade (thrombin)
  • fibrinopeptides + fibrin clot
  • Fibrin degradation
  • Increases vascular permeability , neutrophil chemotaxis
72
Q

what does the clotting pathway do?

A

increase vascular permeability and neutrophil chemotaxis

73
Q

what does the fibrinolytic pathway do?

A

complement activation

74
Q

what does the kinin pathway do?

A

increases vascular permeability
vasodilation
Pain
Smooth muscle contraction

75
Q

steps for kinin pathway

A
  • Endothelial damage
  • Activation of Hageman factor
  • prekallilkrein
  • Kallikrein
  • Kininogen converted to bradykinin
  • increases vascular permeability, vasodilation, pain, smooth muscle contraction
76
Q

kinin, clotting and fibrinolytic pathway all contribute to what type of response?

A

innate

77
Q

define complement

A

group of serum and cell surface proteins

78
Q

role of complement (3):

A

regulate inflammatory and immune responses
acts as opsonins to increase phagocytosis
lyse cells and microorganisms

79
Q

complement components present in what form? in blood

A

inactive prescursors

80
Q

Role of prostaglandins

A

Cause vascular dilation & enhance effect of histamine & bradykinin on vascular permeability

81
Q

role of leukotrienes

A

promote wbc migration into tissues

82
Q

NTKs (natural killer cells) share expression of what?

A

some T cell & some MC/ granulocyte surface markers

83
Q

NKs also have receptor for antibody. This is helpful why?

A

can attcak antibody coated target cells such as tumuor cells - (process called ADCC)

84
Q

ADCC (NKs)

A

antibody dependent cellular cytotoxicity

85
Q

NKs are the same progenitors as T cells but?

A

branch off early with no T cell receptor (specific antigen recognition system)

86
Q

Killing mechanism of NKs

A
  • form pores in target cell membrane by secreted molecules e.g. perforin & granzymes
  • also induce apoptosis
  • kill a range of tumour targets & virally infected cells