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BM 212: Introduction to Immunology > Block E Lecture 1: Hypersensitivity > Flashcards

Block E Lecture 1: Hypersensitivity Flashcards

1
Q

What is inflammation?

A

A biological response of the innate immune system
(Slide 3)

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2
Q

What 3 ways can inflammation be triggered?

A

Pathogens
Damaged cells
Toxin compounds
(Slide 3)

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3
Q

What are the 5 classic signs of inflammation?

A

Heat
Redness
Swelling
Pain
Loss of function
(Slide 4)

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4
Q

What causes the heat and redness signs of inflammation?

A

High blood flow heating the tissue and causing redness caused by increased blood flow and capillary widening (vasodilation)
(Slide 5)

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5
Q

What causes the swelling sign of inflammation?

A

Fluid released into tissues, increased permeability and tenderness due to an increased influx of leukocytes to the site of injury
(Slide 5)

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6
Q

What causes the pain sign of inflammation?

A

Fever and proliferation of leukocytes
(Slide 5)

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7
Q

What causes the loss of function sign of inflammation?

A

Resolution, wound healing and scar tissue preventing movement
(Slide 5)

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8
Q

When does the inflammatory response start?

A

When macrophages and other cells residues in the affected tissues are activated
(Slide 6)

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9
Q

How are macrophages and other cells resident in affect tissues needed to start the inflammatory response activated?

A

By PAMPS and DAMPS to PRRs
(Slide 6)

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10
Q

What are 4 inflammatory mediators?

A

Leukotrienes
Prostaglandins
Platelet activating factors
Histamine
(Slide 6)

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11
Q

What do inflammatory signals secreted by injured tissue (endothelial cells), mast cells and macrophages induce?

A

Vascular changes
(Slide 7)

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12
Q

What are 3 examples of the vascular changes caused by inflammatory mediators secreted by injured tissue, mast cells and macrophages and what do these changes each do?

A

Increased blood flow to area - increasing deliver of beneficial proteins / leukocytes

Increased vascular permeability - allowing plasma proteins to gain entry to interstitial fluid (body fluid between blood and cells)

Complement (C5a) enhancing the process of vasodilation and helping activate endothelial and mast cells resident in tissues
(Slide 7)

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13
Q

Can dendritic cells and macrophages phagocytise bacteria?

A

Yes
(Slide 9)

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14
Q

What 4 cells are the key cellular components of inflammation?

A

Neutrophils
Macrophages
Dendritic cells
Mast cells
(Slide 9)

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15
Q

What do phagocytes do once they enter the area of infection and encounter microbes?

A

They release inflammatory mediators that bring in even more phagocytes
(Slide 11)

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16
Q

What may the inflammatory mediators released by phagocytes induce?

A

Fever
(Slide 11)

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17
Q

What is considered fever in humans?

A

A body temperature greater than 38°C (100.4°F)
(Slide 11)

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18
Q

What 4 things does fever do?

A

Stimulate leukocyte activity
Provide a less hospitable environment for some pathogens
Destroys / inactivates pathogens
Clears area of dead cells, setting the stage for tissue repair
(Slide 11)

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19
Q

What is extravasation of leukocytes highly regulated by?

A

Adhesion molecules
(Notes section of Slide 12)

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20
Q

What 2 things can occurs when the immune system’s strategies to reduce damage to self fail?

A

Auto-immunity and Hypersensitivity
(Slide 14)

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21
Q

What is hypersensitivity?

A

An inappropriate / over-reactive response to antigens that pose little or no threat
(Slide 14)

22
Q

What are the 2 broad classes of hypersensitivity classes?

A

Immediate and delayed hypersensitivity
(Slide 15)

23
Q

What 4 types of classification are in the Gell and Coombs classification of hypersensitivity?

A

Type I, Type II, Type III and Type IV
(Slide 16)

24
Q

What are each of the 4 types of hypersensitivity mediated by?

A

Type I - IgE-mediated
Type II - IgG or IgM-mediated
Type III - Immune complex-mediated
Type IV - T-cell-mediated
(Slide 16)

25
Q

What occurs in Type 1 (IgE mediated) hypersensitivity?

A

IgE is displayed by mast cells and basophils and binds the antigen on second exposure, resulting in degranulation
(Slide 19)

26
Q

What are vasoactive mediators?

A

Substances that can induce changes in the diameter of blood vessels
(Slide 19)

27
Q

Name 3 vasoactive mediators.

A

Answers include:
Histamine
Heparin
Prostaglandins
Leukotrienes
Proteases
(Slide 19)

28
Q

What occurs in the immediate and late phase responses of Type 1 hypersensitivity?

A

Immediate early response occurs due to release of vasoactive compounds, and localised inflammation occurs in the late response due to mediators released
(Slide 20)

29
Q

What is Type II hypersensitivity?

A

Antibody-mediated destruction of cells by IgG and IgM
(Slide 23)

30
Q

What occurs in Type II hypersensitivities?

A

Antibodies target antigens on cells -
IgG or IgM binds to an antigen on the surface of a cell, forming an immune complex, which can activate complement, leading to the destruction of the cell
(Slide 24)

31
Q

What 3 things are classed as type II hypersensitivies?

A

Blood transfusion reactions
Haemolytic disease of the new-born
Autoimmune anaemia
(Slide 24)

32
Q

What is haemolytic disease of the new-born?

A

A haemolytic disease when a Rh- mother is carrying an Rh+ baby
(Slide 25)

33
Q

How can haemolytic disease of the new-born be prevented?

A

By administration of Rhogam at the time of delivery
(Slide 25)

34
Q

How does haemolytic disease of the new-born occur?

A

When an Rh- mother gets pregnant by an Rh+ father, there is a danger of the mother developing a response to the Rh antigen that the foetus has inherited from the father which can lead to the mother rejecting the Rh+ foetus
(Slide 25)

35
Q

How does an Rh- mother produce anti Rh+ antibodies?

A

As red blood cells from the foetus can enter the maternal circulation during pregnancy
(Slide 25)

36
Q

What can these anti Rh+ antibodies produced the the mother do?

A

Cross the placenta into the foetus’s bloodstream and start attacking Fetal blood cells
(Slide 25)

37
Q

What causes Type III hypersensitivity?

A

Immune complex are important for the clearance of antigen by phagocytotic cells - but large number of these can result in tissue damage
(Slide 28)

38
Q

What 3 things determines the severity of Type III hypersensitivity?

A

The level of immune complexes present
The size of the immune complexes
The distribution within the body
(Slide 28)

39
Q

What are 2 possible explanations of how the body fails to clear immune complexes in Type III hypersensitivity?

A

Disorders in the phagocytic machinery or irregularities with the antigen
(Slide 29)

40
Q

What happens when immune complexes are not cleared in type III hypersensitivity?

A

They can be deposited in the blood vessels or tissues and can bind to mast cells, neutrophils and macrophages
(Slide 29)

41
Q

What reaction do immune complexes deposited near the antigen administration site induce?

A

The Arthus reaction
(Slide 31)

42
Q

What is the Arthus reaction?

A

A localised event where large immune complexes precipitate close to the injection site of antigen
(Slide 31)

43
Q

What is type IV hypersensitivity also known as?

A

Delayed-type hypersensitivity
(Slide 33)

44
Q

How long is the delay for a reaction to develop in type IV hypersensitivity?

A

1-2 days
(Slide 33)

45
Q

What 2 phases does Type IV hypersensitivity involve?

A

A sensitisation and an effector phase
(Slide 33)

46
Q

What is a common example of Type IV hypersensitivity?

A

Dermatitis
(Slide 33)

47
Q

What happens after the sensitisation phase of Type IV hypersensitivity?

A

T-cells clonally expand and differentiate into effector T-cells
(Slide 34)

48
Q

What happens in the effector phase of type IV hypersensitivity?

A

During 2nd exposure to the antigen the T-cells secrete IFN-gamma, TNFα and TNF-ß which recruit and activate macrophages which amplifies the response as they are very good at presenting the antigen
(Slide 34)

49
Q

What does heightened phagocytic activity due to type IV delayed hypersensitivity result in?

A

A build up of lytic enzymes from macrophages in the area of infection
(Slide 36)

50
Q

What does a prolonged delayed type hypersensitivity response result in?

A

Visible granuloma
(Slide 36)

51
Q

What is visible granuloma?

A

The continues activation of macrophages which induces them to adhere closely, making them fuse to form multinucleated (more than one nucleus) giant cells which can displace normal tissue cells forming nodules
(Slide 36)

BM 212: Introduction to Immunology (13 decks)

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