Hypersensitivity

Question 1

Examples of innate immunity deficiency

Answer 1

Chronic granulomatous diseases
- Enzymatic defect adversely affecting the production of reactive oxygen species by phagocytes (WBCs)

Leukocyte adhesion deficiency
- Defect in phagocyte trafficking proteins

Question 2

Treatment of bronchial asthma

Answer 2

corticosteroids → reduce inflammation

leukotriene antagonists → relax bronchial smooth muscle, reduce inflammation

phosphodiesterase inhibitors → relax bronchial smooth muscles

Question 3

Treatment of allergic diseases

Answer 3

1. Desensitisation (repeated administration of low doses of allergens) → may inhibit IgE production and increase production of other isotypes; induce T cell tolerance
2. Anti-IgE antibody → neutralises and eliminates IgE
3. Antihistamines → block action of histamines on vessels and smooth muscles
4. Cromolyn → inhibits mast cell degranulation

Question 4

manifestations of type IV hypersensitivity

Answer 4

contact dermatitis

tuberculin skin test

Question 5

contact dermatitis

Answer 5

• Contact-sensitising agent penetrates the skin and binds to self proteins, which are taken up by langerhans’ cells, making self proteins look foreign
• Langerhans’ cells present self peptides haptenated with the contact-sensitising agent to Th1 cells which secrete IFN-gamma and other cytokines
• IFN-gamma acts on epithelial cells → activated keratinocytes secrete cytokines such as IL-1 and TNF-α
• IFN-gamma + IL-1 + TFN-α activate macrophages to secrete mediators of inflammation

Question 6

tuberculin skin test

Answer 6

• Antigen is injected into subcutaneous tissue and processed by local antigen-presenting cells
• Th1 effector cell recognises the antigen and releases cytokines which act on vascular endothelium
• Recruitment of phagocytes and plasma to site of antigen injection causes visible lesion

note: faster process means that it is a repeated exposure