What is Type I Hypersensitivity? Type I hypersensitivity is also called immediate or anaphylactic hypersensitivity. The reaction may affect the skin, eyes, nasopharynx, bronchopulmonary tissues and gastrointestinal tract. Hypersensitivity can cause a variety of symptoms ranging from minor health problems to death. The reaction usually takes 15 to 30 minutes from the time of exposure to the antigen, although it can sometimes have a delayed onset of 10 to 12 hours. (#1) Immediate hypersensitivity is mediated by IgE and the main cellular factor is the mast cell or basophil. The reaction is intensified or modified by platelets, neutrophils and eosinophils. While the mechanism of this reaction is involved in the promoted production of IgE in response to certain antigens, some people are more susceptible to type I hypersensitivity than others and the precise mechanism is not known. However, these individuals have been shown to preferentially produce more TH2 cells that secrete IL-4, IL-5, and IL-13, which promotes IgE class switching. IgE has a very strong affinity for its receptor (Fcε; CD23) on mast cells and basophils. (#1) Successive exposure to the same allergen can cause cell-bound IgE to cross-link and activate the release of many pharmacologically active substances. Cross-linking of the IgE Fc receptor is imperative in mast cell activation; mast cell degranulation is followed by increased Ca2+ influx, which is a crucial process; ionophores that increase cytoplasmic Ca2+ also promote degranulation, while agents that deplete cytoplasmic Ca2+ suppress degranulation. Mast cells can be activated by other stimuli such as exercise, emotional stress, anaphylotoxins. These reactions, mediated by agents without IgE-allergen interaction...... middle of article ......include T lymphocytes and monocytes or macrophages. Cytotoxic T cells cause direct damage while helper T cells secrete cytokines that activate cytotoxic T cells which recruit, activate monocytes and macrophages, which cause the bulk of the damage. (#1) Delayed hypersensitivity lacerations contain primarily monocytes and some T cells. The major lymphokines involved in the delayed hypersensitivity reaction include monocytic chemoattractant factor, interleukin-2, interferon gamma, TNF alpha /beta, etc. (#1) Analytical tests in type IV hypersensitivity include delayed skin reaction and patch test. In vitro tests for delayed hypersensitivity include mitogenic response, lymphocytotoxicity, and IL-2 production. Corticosteroids and other immunosuppressive agents are used in treatment. Diseases associated with type IV hypersensitivity are tuberculin test, poison ivy, and granuloma..