Hypersensitivity revisited

When someone who is allergic to house dust mites starts wheezing they are experiencing a type Ihypersensitivity reaction. Type I reactions occur rapidly and are mediated by IgE antibodies (to the allergen) which bind strongly to the surface of mast cells in the skin. The synthesis of IgE antibodies is triggered by T helper cells (Th 2 cells) which produce a number of inflammatory cytokines in the process. The most important cytokine in these type I responses is interleukin 4.

When the IgE antibodies bind to mast cells they break open and release histamine which causes the clinical symptoms. The clinical response usually stops when the allergen is removed or when theinflammatory response is dampened down by antihistamine drugs or anti-inflammatory drugs. Other type I hypersensitivity reactions include allergic rhinitis, eczema, urticaria, and systemic anaphylaxis.

Type II and type III hypersensitivity reactions are mediated by IgG antibodies. These set off the complement cascade which induces phagocytosis of the allergens. Common examples of these hypersensitivity reactions include reactions to drugs and serum sickness. Type II reactions are directed against antigens on the cell surface; type III reactions are directed against soluble antigens.

Type IV hypersensitivity reactions are mediated by T cells, and tissue damage is caused by macrophages and cytotoxic T cells. Contact dermatitis is a clinical example of a type IV hypersensitivity reaction.