Hypersensitivity Flashcards
Describe each type of hypersensitivity reaction
Type 1 - immediate (IgE)
Type 2 - cell-bound antigen (IgG, IgM)
Type 3 - immune complex (IgG)
Type 4 - delayed (T-cells)
What exposures can cause hypersensitivity?
o Infectious agents
o Environmental substances
o Self-antigens
How can influenza viruses cause hypersensitivity?
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 can dust cause hypersensitivity and what are the antibodies associated with asthma and farmers lung?
- 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
What are the adaptive and innate immune system mediators involved in each hypersensitivity reaction?
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
Describe Type 1 hypersensitivity
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 is IgE secreted?
B cells produce it when co-stimulated with IL-4 (secreted by TH2 cells)
What are allergens?
Antigens that trigger allergic reactions
Peanut allergy is the most common cause of severe allergic reactions - ARA h2 protein
Multiple food allergies - ARA h8
What are degranulating cells?
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)
Describe anaphylaxis
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
Describe allergic rhinitis
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
Describe asthma
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 is allergy treated?
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
Describe type 2 hypersensitivity
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 does the body form anti-A and B antigens against blood?
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