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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
Why is co-stimulation necessary?
This ensures that when a B cell phagocytoses something, it doesn't immediately get to make antibodies for it.
26
What signals do highly immunosuppressive drugs block?
BCR and TCR
27
What triggers co-stimulation?
Innate system fine discrimination
28
What are the four steps of the infection pathway?
1. Infection has to establish in face of innate response 2. Induction of adaptive response 3. Reduce/sterilise infection 4. Immunological memory
29
What type of cell is the effector cell of the dermis?
Phagocytic
30
What protein is responsible for opsinization?
C3b
31
What is the role of C3b?
Opsonisation MAC Recruitment of inflammatory cells
32
What is MAC?
Membrane Attack Complex
33
How does MAC work?
Forms perforations in cell membrane resulting in cell lysis
34
What is degradation?
Breaking down the whole pathogen/antigen into genetic fragments
35
What is diapedeis?
Movement of while blood cells through intact capillary walls into surrounding tissue.
36
What is another term for diapedesis?
Leukocyte extravasatio | Migration
37
What are dendritic cells?
Very specialised phagocytes that can return to lymph nodes with information about infections
38
What are Langerhan cells?
APCs/ Dendritic cells of skin and mucosa
39
What do Langerhan cells contain?
Birbeck granules
40
Where are Langerhan cells most abundant in the skin?
Stratum spinosum
41
What is the role of dendritic cells?
Turn on T cell responses Sense the environment Make a range of cytokines to influence T cell differentiation
42
What class of MHC molecules do dendritic cells have?
MHC II
43
What are high endothelial venues?
Specialised blood vessels for lymphocyte migration
44
How are high endothelial venules generally used by lymphocytes?
Bloodstream -> Lymph nodes
45
What kind of signalling do immune cells use?
Similar to synaptic
46
What happens to T lymphocytes in the process of trapping?
Moved from lymph to bloodstream
47
What is the difference between TH1 and TH2 CD4 T cells?
TH1 bind to macrophages to make more macrophages | TH2 bind to B cells turned APCs to check them/allow them to make antibodies
48
What are the cardinal signs of inflammation?
Heat, Redness, Pain, Swelling
49
Why do the cardinal signs of inflammation come about?
Acute vasodilation of capillaries
50
What are examples of chronic infections?
Autoimmunity and transplant rejection
51
What is a major source of mediators for the immune response?
Liver
52
Why are lipids rapidly synthesised?
They're not dependent on protein synthesis
53
True or false? Cytokines aren't usually dependent on protein synthesis?
False
54
What is the specific mechanism of action for dendritic cells?
Macropinocytosis
55
Where are mast cells usually located?
Next to the vasculature
56
How are prostaglandins made?
Conversion of arachadonic acid to cyclic endoperoxides which get converted into prostaglandins
57
How are leukotrienes made?
Conversion of arachadonic acid into 5-lipoxygenase
58
What are the mediators that resolve inflammation known as?
Lipoxins
59
How are lipoxins made?
Conversion of arachidonate into 15-lipoxygenase
60
What are leukotrienes?
Biologically active compounds made by leukocytes
61
What are the 3 As of NSAIDs?
Anti-inflammatory Analgesic Antipyretic
62
Why isn't paracetamol an NSAID?
It isn't an anti-inflammatory
63
What does aspirin do to COX?
Inactivates both isoforms
64
What part of aspirin's actions is responsible for its 3As?
Acetylates catalytic serine residue on position 529
65
On what levels does aspirin affect COX 2 expression?
Transcriptional and post-transcriptional
66
How does aspirin end up producing lipoxins?
COX 2 acetylation modifies the enzyme so that instead of completing its reaction to make prostaglandins it stops at lipoxins.
67
Which mediators are preformed in secretory granules?
Histamine Serotonin Lysosomal enzymes
68
What are the mediators of acute inflammations that are newly synthesised?
``` Prostaglandins Leukotrienes Platelet-activating factors Activated oxygen species Nitric oxide Cytokines ```
69
What are the side effects associated with chronic use of aspirin?
``` 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
True or false? Swelling of the eyes can occur with chronic aspirin use?
True
71
Is dry cough a side effect of chronic aspirin use?
No
72
What are coxibs?
Selective COX 2 Inhibitors
73
What are coxibs used for?
Rheumatoid arthritis
74
What is a famous example of a coxib?
Vioxx
75
What are NO-NSAIDs?
Nitric oxide -donating NSAID
76
What are SAIDs?
Glucocorticoids
77
What does chronic use of corticosteroids cause?
Toxicity
78
How do mast cells release histamine?
Exocytosis
79
What is the Lewis Triple Response (LTR)?
Reddening, Weal and Flare
80
Why does the Lewis Triple Response occur?
Histamine
81
What is the reddening in LTR caused by?
Vasodilation of small arterioles and pre-capillary vessels
82
What is wheal in LTR caused by?
Increased permeability of post-capillary venules
83
What is wheal in the Lewis Triple Response?
Swelling/ Localised oedma
84
What is flare in the Lewis Triple Response?
Redness extending beyond where you put the foreign object
85
What is flare in LTR caused by?
Release of vasodilators caused by antidromic stimulation of local nerves
86
What is the effect of mast-cell activation and granule release on the GI tract?
Increased fluid secretion and peristalsis -> Expulsion of GI tract contents
87
What is the effect of mast-cell secretion on the eyes, nasal passages and airways?
Decreased diameter and increased mucus secretion -> Congestion and coughing
88
What is the effect of mast-cell secretion on blood vessels?
Increased blood flow and permeability (potentially -> via anaphylaxis)
89
What is immediately released by mast-cells on exposure to infection?
Granules containing histamine TNF alpha Proteases
90
What can immediate secretions from mast cells cause?
Anaphylaxis Acute vomiting Airway constriction
91
What can the secretions released by mast cells (after a few minutes of infection) cause?
Recruitment of lymphocytes like neutrophils
92
What can the secretions released by mast cells (after a few hours of infection) cause?
Class switching from IgG to IgE
93
What is released by mast-cells after a few minutes of infection exposure?
Prostaglandins | Leukotrienes
94
What is released by mast-cells after a few hours of infection exposure?
IL-4 | IL-13
95
What are the effects of histamine after being released from mast cells?
- Bronchoconstriction | - Increasing vascular permeability
96
What are the effects of leukotrienes after being released from mast cells?
- Bronchoconstriction - Increasing vascular permeability - Mucus secretion - Chemotaxis
97
What are the effects of prostaglandins after being released from mast cells?
- Bronchoconstriction - Increasing vascular permeability - Mucus secretion
98
What are the effects of TNF alpha after being released from mast cells?
Tissue injury | Cell recruitment
99
What are the effects of proteases after being released from mast cells?
Tissue injury | Mucus production
100
What is the only mast cell secretion responsible for mucus production?
Proteases
101
What is the only mast cell secretion responsible for cell recruitment?
TNF alpha
102
What is the only mast cell secretion responsible for chemotaxis?
Leukotrienes
103
How does epinephrine deal with anaphylaxis?
Triggers vasoconstriction, increasing blood pressure

Phase I Medicine (46 decks)

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