Hypersensitivity Flashcards

1
Q

Describe each type of hypersensitivity reaction

A

Type 1 - immediate (IgE)

Type 2 - cell-bound antigen (IgG, IgM)

Type 3 - immune complex (IgG)

Type 4 - delayed (T-cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What exposures can cause hypersensitivity?

A

o Infectious agents
o Environmental substances
o Self-antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can influenza viruses cause hypersensitivity?

A

Damages epithelial cells in the respiratory tract which may trigger high levels of cytokine secretion. The cytokines attract leukocytes to the lungs and trigger vascular changes that lead to hypotension and coagulation

In severe influenza, inflammatory cytokines also spill out into the systemic circulation, causing ill effects in remote parts of the body, such as the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can dust cause hypersensitivity and what are the antibodies associated with asthma and farmers lung?

A
  • Dust triggers responses because it is able to enter the lower extremities of the respiratory tract, an area rich in adaptive immune response cells
  • Dust can mimic parasites and may stimulate an antibody response

Asthma and rhinitis - IgE immediate hypersensitivity

Farmers lung - IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the adaptive and innate immune system mediators involved in each hypersensitivity reaction?

A

Type 1 - immediate
Adaptive - IgE
Innate - mast cells, eosinophils

Type 2 - cell-bound antigen
Adaptive - IgG, IgM
Innate - compliment, phagocytes

Type 3 - immune complex
Adaptive - IgG
Innate - compliment, neutrophils

Type 4 - delayed
Adaptive - T-cells
Innate - macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe Type 1 hypersensitivity

A

Mast cells and eosinophils, IgE

The effects are felt within minutes of exposure

Immediate hypersensitivity, allergy

B cells produce it when co-stimulated with IL-4 (secreted by TH2 cells)

Atopy (allergy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is IgE secreted?

A

B cells produce it when co-stimulated with IL-4 (secreted by TH2 cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are allergens?

A

Antigens that trigger allergic reactions

Peanut allergy is the most common cause of severe allergic reactions - ARA h2 protein

Multiple food allergies - ARA h8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are degranulating cells?

A

Release of mediators that cause allergic symptoms

Mast cells are resident in many tissues

Eosinophils migrate to tissues where type I hypersensitivity reaction is

Mast cells initiate allergic symptoms after allergen and IgE interact

Mast cells have receptors for IgE and FcEµRI (also IgE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe anaphylaxis

A

Low BP
Angioedema
Airway obstruction

Caused by mast cells producing prostaglandins and leukotrienes. The result is vasodilation and increased vascular permeability. Shift of fluids from the vascular to the extra-vascular space resulting in a fall in vascular tone and severe drop in blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe allergic rhinitis

A

Inhaled allergens stimulate mast cells in the nasal mucosa and subsequent vasodilation and oedema in the nose causes nasal stuffiness and sneezing

Leukotrienes increase mucus secretion, which causes the discharge characteristic of allergic rhinitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe asthma

A

Increased mucus secretion in asthma and contributes to the airflow obstruction

In the lungs, leukotrienes cause smooth muscle contraction, which has the most dramatic effects on airflow reduction

The symptoms improve after an hour or so as the immediate response dies down

Several hours after the acute episode, the airflow in the bronchi may deteriorate again, reflecting the migration of leukocytes into the bronchi in response to chemokines

The late phase may last several hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is allergy treated?

A

Beta-agonists - Mimic the effects of the sympathetic nervous system and work mainly by preventing smooth bronchial muscle contraction in asthma

Epinephrine (adrenaline) - Stimulates adrenergic receptors, decreases vascular permeability, increases blood pressure, and reverses airway obstruction

Antihistamines - block specific histamine receptors and have an important role in allergies that affect the skin, nose, and mucus membranes

Specific receptor antagonists - block the effects of leukotrienes e.g. montelukast LTRA

Corticosteroids - can prevent the immediate hypersensitivity reaction, the late phase, and chronic allergic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe type 2 hypersensitivity

A

IgG or IgM reacting with antigen present on the surface of cells leading to tissue damage

The bound Ig interacts with complement or with Fc receptor on macrophages

Opsonisation of target cells

Immune mediated haemolysis

Takes several hours

Drug-induced haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does the body form anti-A and B antigens against blood?

A

A and B blood group antigens are oligosaccharides on the surface of RBCs

Similar to molecules expressed by bacteria

Antibodies recognize A and B

Anti-A and Anti-B are IgM antibodies naturally occurring

Individuals with O group have both antibodies from birth regardless of exposure

Antibodies produced against these antigens can cause type II hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does alloimmune haemolysis occur?

A

Rhesus negative mother has rhesus positive baby

During labour, the foetal blood miss with the mother

The mother produces IgG antibodies

Thus, if the mother is pregnant with another rhesus positive baby, the antibodies will leak across the placenta and attack the baby’s RBCs

The baby has no effect on the mother as she has antibodies

17
Q

How can autoimmune haemolysis occur?

A

Autoimmune haemolytic anaemia could be induced by infections or drugs

Part of a systematic autoimmune disease (SLE)

Autoantibodies produces by malignant B cells

18
Q

What is Goodpasture syndrome?

A

IgG autoantibodies bind a glycoprotein in the basement membrane of the lung and glomeruli

Anti–basement membrane antibody activates complement, which can trigger an inflammatory response

19
Q

Describe type 3 hypersensitivity

A

Immune complex disease, IgG

Immune complexes of antigen and antibody form and cause damage at the site of production or circulate and cause damage elsewhere

Immune complexes take some time to form and to initiate tissue damage

(ANTIBODY+ANTIGEN)

20
Q

How do immune complexes form and how are they usually disposed of?

A

At low levels of antibody, each antigen molecule binds several immunoglobulin molecules

When antibody and antigen levels are approximately equal, or antibody levels are slightly in excess, large complexes can form

Complement breaks down large complexes

Complement Receptor 1 (CR1) transfers Complexes to Phagocytes

21
Q

What happens when the complement fails to remove the complex?

A

Activation of the innate immune system

22
Q

How can immune complexes affect the kidney?

A

Glomerulonephritis

a) Nephrotic syndrome (protein leaks into urine) with gradual development of renal failure
b) Nephritis with rapid onset renal failure, blood and protein in the urine and hypertension

(farmer’s lung is also type 3)

23
Q

Describe type 4 hypersensitivity

A

The slowest form of hypersensitivity is that mediated by T cells

This can take 2 to 3 days to develop

24
Q

How are type 4 reactions initiated and what are the consequences?

A

Delayed hypersensitivity reactions are initiated when tissue macrophages recognise danger signals and initiate an inflammatory response

Dendritic cells loaded with antigen migrate to local lymph nodes, where they present antigen to T cells

Specific T-cell clones proliferate in response to antigens, which migrate to the site of inflammation

Tumour necrosis factor (TNF) is secreted by both macrophages and T cells and stimulates much of the damage in delayed hypersensitivity

(dendritic cells = antigen-presenting cells)

25
Q

What are the antigens that drive rheumatoid arthritis?

A

Citrullinated protiens

Autoreactive T cells and B cells can recognize citrullinated proteins

The result is production of antibodies against citrullinated protein

These are referred to as anti–cyclic citrullinated peptide (CCP) antibodies

26
Q

Describe the pathogenesis of RA

A

The synovium becomes infiltrated by T cells (TH1 and TH17) and macrophages

TNF and IL-17 attract and activate neutrophils that cause damage to the synovium

Osteoclasts are activated and destroy bone at the joint margins, creating erosions

Persistent IL-6 secretion triggers an acute-phase response

27
Q

Describe the pathogenesis of MS

A

Chronic, disabling neurologic disease

Initially in MS, acute attacks occur during which inflammatory lesions consisting of TH1 and TH17 cells and macrophages develop in the affected nervous tissue

The inflammatory lesions cause the reversible, relapsing disability typical of early MS

Although active inflammation is present in the vicinity, myelin loss impairs the ability of neurons to conduct impulses, resulting in neurologic symptoms

28
Q

how is delayed hypersensitivity managed?

A

Prevention through avoiding antigens

Anti-inflammatory drugs
o	NSAID
o	Corticosteroids
o	Drugs that block TNF and IL-6
o	Antibodies against B cells

Immunosuppressive drugs