Essay --

What is type I hypersensitivity? Type I hypersensitivity is also called immediate or anaphylactic hypersensitivity. The reaction may include skin, eyes, nasopharynx, bronchopulmonary tissues and gastrointestinal tract. Hypersensitivity may cause a variety of symptoms from minor health problems to death. The reaction usually takes 15 - 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset from 10 - 12 hours. (#1) Immediate hypersensitivity is mediated by IgE and the primary 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 favored production of IgE in response to certain antigens. Some people are more susceptible to type I hypersensitivity then others and the precise mechanism is not known. However, it has been shown that such individuals preferentially produce more of TH2 cells that secrete IL-4, IL-5 and IL-13 which in turn favor IgE class switch. IgE has very high affinity for its receptor (FcÃŽ µ; CD23) on mast cells and basophils. (#1) A succeeding exposure to the same allergen can cause the cross links of the cell-bound IgE and activates the release of numerous pharmacologically active substances. Cross-linking of IgE Fc-receptor is imperative in mast cell activating; mast cell degranulation is followedby increased Ca2+ influx, which is a crucial process; ionophores which increase cytoplasmic Ca2+ also promote degranulation, while agents that deplete cytoplasmic Ca2+ suppress degranulation. Mast cells may be activated by other stimuli such as exercise, emotional stress, anaphylotoxins. These reactions, mediated by agents without IgE-allergen interacti... ...nclude T lymphocytes and monocytes or macrophages. Cytotoxic T cells cause direct damage while helper T cells secrete cytokines which activate cytotoxic T cells that recruit, activate monocytes and macrophages, which cause the bulk of the damage.(#1) The delayed hypersensitivity lacerations mainly contain monocytes and some T cells. Major lymphokines involved in delayed hypersensitivity reaction include monocyte chemotactic factor, interleukin-2, interferon-gamma, TNF alpha/beta, etc. (#1) Analytical tests in type IV hypersensitivity include delayed cutaneous reaction and patch test. In vitro tests for delayed hypersensitivity include mitogenic response, lympho-cytotoxicity and IL-2 production. Corticosteroids and other immunosuppressive agents are used in treatment. The diseases associated with type IV hypersensitivity are tuberculin test, poison ivy and granuloma.