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POM 4 Immunology > 4.8 Hypersensitivity > Flashcards

4.8 Hypersensitivity Flashcards

1
Q

What is meant by hypersensitivity?

A

Immune reaction that damages the body rather than protecting it from infection

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2
Q

What is the name of type I hypersensitivity?

A

Immediate/anaphylactic hypersensitivity

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3
Q

What are type I hypersensitivity reactions mediated by?

A

IgE antibodies

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4
Q

What is type I hypersensitivity triggered by?

A

Multivalent environmental antigens (allergens)

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5
Q

What 2 phases does type I hypersensitivity occur in?

A

Sensitisation

Re-exposure leading to anaphylaxis

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6
Q

Which 3 factors influence the initial sensitisation of the immune response to allergens?

A

Genetics, age, environment

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7
Q

Outline the sensitisation phase of type I hypersensitivity

A

APC present antigen and co-stimulatory molecule to T cell

Naive T cell becomes primed and differentiates into TH2 cell

TH2 cells release IL4 and 12 to promote class switching from IgM to IgE, and IL5 which activates eosinophils

IgE then bind FcE receptors on mast cells

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8
Q

Outline what happens in second exposure in type I hypersensitivity

A

Allergen binds to IgE on mast cells, crosslinking two IgE molecules

This causes rapid degranulation, releasing pro inflammatory mediators (histamines, cytokines, leukotrienes, prostaglandins)

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9
Q

What effects does histamine have?

A

Binds to H1 receptors

Causes bronchoconstriction, vasoconstriction, increased vascular permeability

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10
Q

What effects do leukotrienes have?

A

Smooth muscle contraction

Recruit neutro/eosinophils/mast cells after allergen is cleared

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11
Q

What happens if an allergen encounters cell bound IgE?

A

Rapid cross linking of IgE and degranulation of the mast cell

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12
Q

What happens in the early phase of type I hypersensitivity?

A

Effects of molecules released in mast cell degranulation

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13
Q

When does the early phase of type I hypersensitivity occur?

A

Few minutes after second exposure

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14
Q

What happens in the later phase of type I hypersensitivity?

A

Recruitment of neutrophils

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15
Q

When does the later phase of type I hypersensitivity occur?

A

Within a few hours

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16
Q

What happens in the late phase of type I hypersensitivity and when?

A

Eosinophils are recruited and TH2 cells are present

3-4 days after exposure

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17
Q

Which of an anaphylactic shock reaction or immune complex reaction requires more antigen to trigger?

A

Immune complex requires more antigen

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18
Q

List 3 treatments for type I hypersensitivity

A

Antihistamines – reduce bronchoconstriction and vascular permeability

Corticosteroids – decrease inflammatory response

Adrenaline – cause vasoconstriction

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19
Q

What causes anaphylactic shock?

A

Decrease in blood supply to vital organs (e.g. the brain) due to increased vascular permeability and increased airway constriction

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20
Q

What is the name of type II hypersensitivity?

A

Antibody mediated cytotoxic hypersensitivity

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21
Q

What does type II hypersensitivity involve?

A

The destruction of cells/tissue by IgG or IgM antibodies that bind to antigens present on the surface of normally healthy cells

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22
Q

What are examples of type II hypersensitivity reactions?

A
  1. Graves disease – antibodies bind to thyrotrophin receptor resulting in the over production of thyroid hormones
  2. Haemolytic disease of newborn – maternal antibodies can cross the placenta and destroy fetal red blood cells
  3. Immune thrombocytopenia – antibodies develop against platelets
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23
Q

What are the three mechanisms by which type II hypersensitivity reactions can occur?

A
  1. Anti-receptor activity
  2. Antibody dependant cell mediated cytotoxicity
  3. Classical activation of the complement cascade
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24
Q

Outline the first mechanism of complement activation in type II hypersensitivity

A

IgM/IgG binds an antigen that is bound to the surface of a healthy cell and activates complement

C1 binds Fc region of antibody and recruits other complement proteins

The proteins that are cleaved are chemotactic – attract neutrophils

Neutrophils degranulate and release enzymes that produce ROS, causing cell death

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25
What enzymes do neutrophils release when they degranulate?
Myeloperoxidase, peroxidase, proteinase 3
26
Outline the second mechanism of complement activation in type II hypersensitivity
Complement proteins form membrane attack complexes MACs create holes in the cell membrane, causing cell death by water influx
27
Outline the third mechanism of complement activation in type II hypersensitivity
**C3b** binds **IgG** antibodies coating a cell Cell becomes **opsonised** and targeted for phagocytosis Antibody-antigen complex and cell encounters **phagocytes** in the spleen Phagocyte binds **Fc tail** or **C3b**, engulfing the cell
28
Outline antibody dependent cell-mediated cytotoxicity as a cytotoxic mechanism of type II hypersensitivity
NK cells recognise the antigen-antibody complex, specifically the **Fc tail** Thus they release **granules** that contain **perforin** **Perforin** forms pores in the cell membrane which allow **granzymes and granulysin** to enter and trigger **apoptosis** Inflammatory mediators, chemokines and cytokines are also released
29
Outline antibody-mediated cellular dysfunction
Antibody stops antigen from binding receptor
30
How does antibody-mediated cellular dysfunction work in **myasthenia gravis**?
Antibody blocks Ach receptors, thus muscles weaken over time
31
How does antibody-mediated cellular dysfunction work in graves disease?
Antibody targets and binds TSH receptors on thyroid follicular cells, causing **overproduction** of thyroid hormone
32
How does type 2 hypersensitivity cause tissue damage?
Local or systemic inflammation Cell depletion thus loss of function Imbalance in organ function
33
How do you test for autoimmune haemolytic anemia?
Direct coomb's test Antibodies are separated from plasma and mixed with **coomb's reagent** which is **anti-human globulin** (antibodies against human antibodies) If agglutination occurs, this indicates **presence of antibody**
34
What happens in type III hypersensitivity?
When immune complexes cannot be cleared and are thus deposited in blood vessel walls and tissue, causing **inflammation** and **tissue damage**
35
What is an immune complex?
**Soluble** antigens bound to antibody (i.e. **non-cell bound** antigen-antibody complexes)
36
Why do immune complexes deposit in blood vessel basement membranes?
The small complexes are **less immunogenic**, thus less attracted to macrophages and less easily removed
37
What is the difference between complement activation in type 2 and type 3 hypersensitivty?
Type III uses complement proteins in **large amounts** compared to type II
38
What issues can type III hypersensitivity lead to?
Fever, rash, protein in blood, joint pain Glomerulonephritis – kidney Arthritis – joints Vasculitis – blood vessel walls
39
What effect do C3 and C4 have in type III hypersensitivity?
They act as chemokines by attracting neutrophils to the side
40
What do neutrophils do when they arrive at the immune complexes in type III hypersensitivity?
They degranulate and result in tissue necrosis and vasculitis
41
What happens in systemic lupus erythmatosus?
IgG is produced against **DNA self-antigens** released from damaged cells Thus IgG-DNA autoantigen complexes form and remain in blood vessels, depositing on the **basement membrane** When deposited, they activate the complement system
42
What happens when complement is activated in systemic lupus erythmatosus?
Complement proteins act as: **Anaphylatoxins** – increase vascular permeability, leading to **oedema** **Chemokines** – recruit neutrophils which degranulate, releasing enzymes that produce **ROS**, causing **vasculitis**
43
What types of antigens cause type 3 hypersensitivity?
Autoantigens Foreign antigens (e.g. from persistent infection)
44
Describe serum sickness
Patient given serum with **anti-venom antibodies** Exposure to foreign antibody in serum triggers B cells to differentiate into plasma cells and **produce IgG** against the **foreign antibody** If the serum is given a second time, IgG forms **immune complexes** with the **anti-venom antibodies**, causing **vasculitis** and **tissue necrosis**
45
What is a membrane attack complex?
Fragments of the complement system form a complex which attaches to the cell surface membrane This creates a channel that disturbs the osmotic integrity of the cell, causing **lysis**
46
Why do immune complexes not initiate complement cascade?
Classical complement pathway involves formation of MAC which occurs in cell walls, whilst immune complexes are **free floating**
47
What are the primary cells involved in type IV hypersensitivity reactions?
T cells
48
What causes type IV hypersensitivity?
CD8 T cells releasing cytotoxic granules CD4 T cells releasing cytokines APCs presenting antigens
49
Outline the sensitisation phase in type IV hypersensitivity
Dendritic cells carry antigen to draining lymph node CD4+ T cells recognise antigen and **bind MHCII** with **TCR and CD4 receptor** Dendritic cell releases **interleukins**, causing differentiation into **Th1 cells** **Th1 cells** release **IL-2** for the proliferation of other T cells and **IFN-gamma** for macrophage activation
50
What do activated macrophages do in type IV hypersensitivity?
Release **pro-inflammatory cytokines**, causing leaky endothelial barriers and immune cell recruitment Release **lysosomal enzymes**, **complement proteins** and **ROS**, causing tissue damage
51
What's the most common example of type IV hypersensitivity and what happens?
Contact dermatitis due to poison ivy Small molecules **urushiol** acts as hapten and binds proteins in skin Upon re-exposure, memory T cells release **cytokines** that promote **pro-inflammatory activation** of macrophages, causing oedema, swelling and lesions
52
What do active macrophages release?
Pro-inflammatory cytokines like TNF, IL-1 and IL-6
53
Which Interleukin has an autocrine effect?
IL-2
54
The test for what infection is conducted via the means of a type 4 hypersensitivity reaction?
Tuberculin skin test, where a protein from **mycobacterium tuberculosis** is injected into the skin In a positive test – TB-specific TH1 cells migrate to site of injection, cause **induration** (skin becomes thick and hard)
55
Why are type IV hypersensitivity reactions called the delayed type?
It takes 48-72 hours to recruit TH1 cells to the site
56
In which auto-immune disease do patients develop IgGs against DNA or proteins present in the nucleus, forming persistent immune complex deposits and a variety of pathologies?
Systemic lupus erythematosus
57
What symptoms can immune complexes not being efficiently cleared lead to?
Symptoms such as fever, rashes, joint pain or protein in the urine
58
What needs to occur before T cells can initiate type IV?
Sensitisation phase where antigen is presented to naive T cells by antigen presenting dendritic cells Results in the generation of antigen specific memory T cells
59
What systemic diseases are type IV hypersensitivity involved in?
Multiple sclerosis – Th1 cells damage myelin around nerve fibres Inflammatory bowel disease – Th1 cells cause inflammation in intestinal lining
60
Give an example where TH2 cells cause type IV hypersensitivity
Asthma, where allergens cause Th2 overreaction This produces soluble mediators, leading to bronchoconstriction
61
What other antigens can cause type IV hypersensitivity?
Nickel salts, hair dyes, intracellular pathogens
62
Give 3 examples where CD8+ T cells cause type IV hypersensitivity
Type 1 diabetes mellitus – attacks pancreatic islet cells Hashimoto's thyroiditis – attacks thyroid epithelial cells Graft rejection – destruction of transplanted cells

POM 4 Immunology (14 decks)

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