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Author: Arthur R. Rabson, M.D.

1. Summary

1.1. Type I - Immediate Hypersensitivity

IgE-mediated, e.g., hay fever or allergic rhinitis; asthma; food allergy; atopic eczema.

IgE attaches to mast cells or basophils which may degranulate on second exposure to the specific antigen.

  • Preformed mediators: histamine, ECF-A, NCF-A
  • Newly formed mediators
    • Platelet activating factor
    • Arachidonic acid metabolites
      • leukotrienes
      • prostaglandins
  • Late acting mediators
    • Cytokines including TNF, IL-1, IL-3, and IL-4. These cytokines are released directly from mast cells and infiltrating T-cells and are responsible for the late phase inflammatory reaction.
  • Release of inflammatory mediators from infiltrating eosinophils, neutrophils, and T-cells

Diagnosis: History, skin testing, laboratory measurement of specific IgE antibodies.

Approach to a dental patient with a history of reaction to a local anesthetic.

Approach to therapy: Acute allergic reactions. Longstanding allergic disease.

1.2. Type II - Hypersensitivity

  • Abnormal antibodies directed to a target organ cause damage either by activating complement or by attracting phagocytic cells which damage the surrounding tissue.
  • Transfusion reactions
  • Autoimmune hemolytic anemia
  • Goodpastures syndrome
  • Anti-receptor antibody disease. In these cases, the abnormal antibody is directed to a receptor on a cell surface. The receptor may be blocked by the antibody (e.g., myasthenia gravis) or activated by it (e.g., Grave's Disease-thyrotoxicosos).

1.3. Type III - Hypersensitivity (immune complex disease)

Circulating immune complexes are normally removed by cells of the reticuloendothelial system. Under certain circumstances, the complexes may accumulate and deposit in the small vessels of organs such as the kidney, skin or joints. Such trapped complexes will activate the complement system, and the generation of C3a and C5a may attract neutrophils to the site where they adhere to the complexes and attempt to phagocytose them. This is often unsuccessful and the neutrophil may discharge its contents extracellularly, resulting in tissue injury.

Localized immune complex disease

  • Arthus reaction

Generalized immune complex disease

  • Systemic lupus erythematosis
  • Serum sickness
  • Rheumatoid arthritis

1.4. Type IV - Hypersensitivity (delayed hypersensitivity)

  • Manifestation of cell-mediated immunity associated with an increased reactivity to a specific antigen, mediated not by antibodies but by T-cells. The reaction is delayed (24-48 hours) and tissue damage is produced by infiltrating T-cells and macrophages with subsequent release of pro-inflammatory cytokines. The ultimate result of the reaction is healing, fibrosis or granuloma formation.
  • Contact dermatitis
  • Tuberculin test
  • Tissue damage observed in a number of chronic infectious diseases: deep fungal infections, tuberculosis, leprosy.