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Phase I Medicine > B4 Innate vs. Adaptive Immunity > Flashcards

B4 Innate vs. Adaptive Immunity Flashcards

1
Q

What is the difference between antigens and immunogens?

A

Antigens - anything that can bind to an antibody.

Immunogens- anything that can illicit an immune response after binding to an antibody.

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2
Q

What is the difference between different epitope structures in antibodies?

A

Variable regions

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3
Q

What is ‘Fab’ on antibody molecular models?

A

Combination of light chains

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4
Q

What is ‘Fc’ on antibody molecular models?

A

Combination of heavy chains

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5
Q

What is affinity of antibodies?

A

How good the binding site is for binding antigens

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6
Q

What is avidity of antibodies?

A

How much more effectively you bind things with more receptors

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7
Q

Why is there a hinge in the structure of antibodies?

A

To change and give extreme flexibility of the structure

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8
Q

What are the four ways that allow for an infinite number of different antibodies?

A

Germ line diversity of genes
Combinatorial Diversity
Junctional Diversity
Somatic Hypermutation

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9
Q

What are the components of somatic recombination?

A

Combinatorial diversity

Junctional diversity

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10
Q

When does somatic hypermutation occur?

A

During an ongoing immune response

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11
Q

What is somatic recombination?

A

Joining together lots of different portions of genes that we already have in different orders

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12
Q

What is the term for changing the function of antibody when it gets to the site of infection and realises it has to do something else?

A

Class switching

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13
Q

What allows for class switching?

A

Somatic hypermutation

Cytokines

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14
Q

Why does clonal selection exist?

A

We can’t afford to have one gene for each antibody

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15
Q

True or false? Cytokines can induce class switching?

A

True

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16
Q

What is positive selection?

A

If you pass each checkpoint, you survive and divide.

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17
Q

What is negative selection?

A

If you fail a check point you get killed off.

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18
Q

How many T cells die in the thymus via negative selection?

A

98%

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19
Q

True or false? B cells and T cells recognise the same part of the antigen?

A

False
B cells use Ab
T cells use TCR

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20
Q

How do B cells recognise antigens?

A

Ab to recognise their complementary conformational epitopes

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21
Q

How do T cells recognise antigens?

A

TCR to recognise linear epitopes or enzymatically digested bits from B cell antigen processing

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22
Q

What is central tolerance?

A

How newly developing T cells and B cells are rendered non-reactive to self

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23
Q

What is the purpose of MHC molecules?

A

To identify small fragments of antigens and shuttle them out to the surface

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24
Q

What is co-stimulation?

A

Adding another checkpoint for B lymphocytes

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25
Q

Why is co-stimulation necessary?

A

This ensures that when a B cell phagocytoses something, it doesn’t immediately get to make antibodies for it.

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26
Q

What signals do highly immunosuppressive drugs block?

A

BCR and TCR

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27
Q

What triggers co-stimulation?

A

Innate system fine discrimination

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28
Q

What are the four steps of the infection pathway?

A
  1. Infection has to establish in face of innate response
  2. Induction of adaptive response
  3. Reduce/sterilise infection
  4. Immunological memory
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29
Q

What type of cell is the effector cell of the dermis?

A

Phagocytic

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30
Q

What protein is responsible for opsinization?

A

C3b

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31
Q

What is the role of C3b?

A

Opsonisation
MAC
Recruitment of inflammatory cells

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32
Q

What is MAC?

A

Membrane Attack Complex

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33
Q

How does MAC work?

A

Forms perforations in cell membrane resulting in cell lysis

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34
Q

What is degradation?

A

Breaking down the whole pathogen/antigen into genetic fragments

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35
Q

What is diapedeis?

A

Movement of while blood cells through intact capillary walls into surrounding tissue.

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36
Q

What is another term for diapedesis?

A

Leukocyte extravasatio

Migration

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37
Q

What are dendritic cells?

A

Very specialised phagocytes that can return to lymph nodes with information about infections

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38
Q

What are Langerhan cells?

A

APCs/ Dendritic cells of skin and mucosa

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39
Q

What do Langerhan cells contain?

A

Birbeck granules

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40
Q

Where are Langerhan cells most abundant in the skin?

A

Stratum spinosum

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41
Q

What is the role of dendritic cells?

A

Turn on T cell responses
Sense the environment
Make a range of cytokines to influence T cell differentiation

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42
Q

What class of MHC molecules do dendritic cells have?

A

MHC II

43
Q

What are high endothelial venues?

A

Specialised blood vessels for lymphocyte migration

44
Q

How are high endothelial venules generally used by lymphocytes?

A

Bloodstream -> Lymph nodes

45
Q

What kind of signalling do immune cells use?

A

Similar to synaptic

46
Q

What happens to T lymphocytes in the process of trapping?

A

Moved from lymph to bloodstream

47
Q

What is the difference between TH1 and TH2 CD4 T cells?

A

TH1 bind to macrophages to make more macrophages

TH2 bind to B cells turned APCs to check them/allow them to make antibodies

48
Q

What are the cardinal signs of inflammation?

A

Heat, Redness, Pain, Swelling

49
Q

Why do the cardinal signs of inflammation come about?

A

Acute vasodilation of capillaries

50
Q

What are examples of chronic infections?

A

Autoimmunity and transplant rejection

51
Q

What is a major source of mediators for the immune response?

A

Liver

52
Q

Why are lipids rapidly synthesised?

A

They’re not dependent on protein synthesis

53
Q

True or false? Cytokines aren’t usually dependent on protein synthesis?

A

False

54
Q

What is the specific mechanism of action for dendritic cells?

A

Macropinocytosis

55
Q

Where are mast cells usually located?

A

Next to the vasculature

56
Q

How are prostaglandins made?

A

Conversion of arachadonic acid to cyclic endoperoxides which get converted into prostaglandins

57
Q

How are leukotrienes made?

A

Conversion of arachadonic acid into 5-lipoxygenase

58
Q

What are the mediators that resolve inflammation known as?

A

Lipoxins

59
Q

How are lipoxins made?

A

Conversion of arachidonate into 15-lipoxygenase

60
Q

What are leukotrienes?

A

Biologically active compounds made by leukocytes

61
Q

What are the 3 As of NSAIDs?

A

Anti-inflammatory
Analgesic
Antipyretic

62
Q

Why isn’t paracetamol an NSAID?

A

It isn’t an anti-inflammatory

63
Q

What does aspirin do to COX?

A

Inactivates both isoforms

64
Q

What part of aspirin’s actions is responsible for its 3As?

A

Acetylates catalytic serine residue on position 529

65
Q

On what levels does aspirin affect COX 2 expression?

A

Transcriptional and post-transcriptional

66
Q

How does aspirin end up producing lipoxins?

A

COX 2 acetylation modifies the enzyme so that instead of completing its reaction to make prostaglandins it stops at lipoxins.

67
Q

Which mediators are preformed in secretory granules?

A

Histamine
Serotonin
Lysosomal enzymes

68
Q

What are the mediators of acute inflammations that are newly synthesised?

A 
Prostaglandins
Leukotrienes
Platelet-activating factors
Activated oxygen species
Nitric oxide
Cytokines
69
Q

What are the side effects associated with chronic use of aspirin?

A 
Swelling of eyes, face, lips, tongue or throat
Tinnitus 
Loss of hearing
Wheezing
Difficulty breathing
Hoarseness
Fast breathing
Tachycardia
Hives
Cold clammy skin
Melaena
GI complaints
70
Q

True or false? Swelling of the eyes can occur with chronic aspirin use?

A

True

71
Q

Is dry cough a side effect of chronic aspirin use?

A

No

72
Q

What are coxibs?

A

Selective COX 2 Inhibitors

73
Q

What are coxibs used for?

A

Rheumatoid arthritis

74
Q

What is a famous example of a coxib?

A

Vioxx

75
Q

What are NO-NSAIDs?

A

Nitric oxide -donating NSAID

76
Q

What are SAIDs?

A

Glucocorticoids

77
Q

What does chronic use of corticosteroids cause?

A

Toxicity

78
Q

How do mast cells release histamine?

A

Exocytosis

79
Q

What is the Lewis Triple Response (LTR)?

A

Reddening, Weal and Flare

80
Q

Why does the Lewis Triple Response occur?

A

Histamine

81
Q

What is the reddening in LTR caused by?

A

Vasodilation of small arterioles and pre-capillary vessels

82
Q

What is wheal in LTR caused by?

A

Increased permeability of post-capillary venules

83
Q

What is wheal in the Lewis Triple Response?

A

Swelling/ Localised oedma

84
Q

What is flare in the Lewis Triple Response?

A

Redness extending beyond where you put the foreign object

85
Q

What is flare in LTR caused by?

A

Release of vasodilators caused by antidromic stimulation of local nerves

86
Q

What is the effect of mast-cell activation and granule release on the GI tract?

A

Increased fluid secretion and peristalsis -> Expulsion of GI tract contents

87
Q

What is the effect of mast-cell secretion on the eyes, nasal passages and airways?

A

Decreased diameter and increased mucus secretion -> Congestion and coughing

88
Q

What is the effect of mast-cell secretion on blood vessels?

A

Increased blood flow and permeability (potentially -> via anaphylaxis)

89
Q

What is immediately released by mast-cells on exposure to infection?

A

Granules containing histamine
TNF alpha
Proteases

90
Q

What can immediate secretions from mast cells cause?

A

Anaphylaxis
Acute vomiting
Airway constriction

91
Q

What can the secretions released by mast cells (after a few minutes of infection) cause?

A

Recruitment of lymphocytes like neutrophils

92
Q

What can the secretions released by mast cells (after a few hours of infection) cause?

A

Class switching from IgG to IgE

93
Q

What is released by mast-cells after a few minutes of infection exposure?

A

Prostaglandins

Leukotrienes

94
Q

What is released by mast-cells after a few hours of infection exposure?

A

IL-4

IL-13

95
Q

What are the effects of histamine after being released from mast cells?

A
  • Bronchoconstriction

- Increasing vascular permeability

96
Q

What are the effects of leukotrienes after being released from mast cells?

A
  • Bronchoconstriction
  • Increasing vascular permeability
  • Mucus secretion
  • Chemotaxis
97
Q

What are the effects of prostaglandins after being released from mast cells?

A
  • Bronchoconstriction
  • Increasing vascular permeability
  • Mucus secretion
98
Q

What are the effects of TNF alpha after being released from mast cells?

A

Tissue injury

Cell recruitment

99
Q

What are the effects of proteases after being released from mast cells?

A

Tissue injury

Mucus production

100
Q

What is the only mast cell secretion responsible for mucus production?

A

Proteases

101
Q

What is the only mast cell secretion responsible for cell recruitment?

A

TNF alpha

102
Q

What is the only mast cell secretion responsible for chemotaxis?

A

Leukotrienes

103
Q

How does epinephrine deal with anaphylaxis?

A

Triggers vasoconstriction, increasing blood pressure

Phase I Medicine (46 decks)

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