Kristen Magliola 12/1/13 BIO 414 Allergies When foreign antigens possess structures similar to host structures, the immune system can be tricked into attacking itself. This problem is otherwise known as an allergic hypersensitive reaction. The antigen that causes the reaction is called an allergen. So altogether allergies are caused by allergens. There are four different types of allergic/ hypersensitivity reactions. They include: Type II, III hypersensitivity, and I. Last but not least Type IV is cell- mediated hypersensitive. Type I hypersensitivity is otherwise known as IgE mediated hypersensitivity. It usually takes about 2-30 min for the reaction to occur and the host has to be exposed to the allergen twice. This kind of sensitivity can also be referred to as immediate or anaphylactic hypersensitivity. This reaction is usually the most common and it occurs due to excess IgE targeting the antigen. The skin, eyes, nasopharynx(nose) bronco pulmonary tissues( lungs/ asthma) and gastrointestinal tract are usually involved. For example when an individual is exposed (ie bee sting allergy) the smooth muscle contracts and the capillaries dilate due to the release of pharmacologically active substances. To break it down even further the primary cellular component in this hypersensitivity is the mast cell or basophil. The reactions are then amplified by platelets, neutrophils and eosinophils. Altogether the mast cells are mostly made up of eosinohils. As stated above excess IgE is produced in response to the antigen so exposure to the same allergen cross links the cell bound IgE and triggers the release of active substances. This is important in triggering the basophil or mast cells. Basophil degranulation is preceded by increased calcium. Ionophores also promote degrnaulation. Agents that decrease cytoplasmic calcium suppress degranulation. There are also many mediators involved in immediate hypersensitivity. To name a few, they include histamine, tryptase, kininogenase, ECF-A, Leukotriene B-4, C4, D4, Prostoglandins D2, and PAF. Other stimuli such as exercise, stress, chemicals, and anaphylotoxins can also trigger mast cells. These reactions are not considered hypersensitive reactions because they are mediated by agents without a IgE allergen interaction. SO how do they work? They are amplified by platelet activation factors. This causes platelet aggregation and releases amines. These amines are: histamine, heparin, and vasoactive. Cyclic nucleotides also play a role in immediate hypersensitivity. Subtances which alter camp and cGMP levels alter allergic symptoms. Increasing cAMP relieves symptoms and vice versa. Treatment for immediate hypersensitivity includes antihistamines, leukotriene receptor blockers, chromolyn sodium, inhibitors of cyclooxygenase pathway, inhalers/ bronchodilators, Thophylline, and IgG antibodies against Fc potions of IgE. Type II hypersensitivity is otherwise known as cytotoxic hypersensitivity. It is also more severe than type I and takes 5-8 hrs to be initiated. In this case the organs and tissues are affected. Antibodies of IgM and IgG play a big role in this type of reaction. A typical example of type II hypersensitivity is a mismatched blood transfusion. In this case the interaction of antibodies and surface antigens of the cells are followed by complement-assisted lysis of these cells. To sum it up, in antibody-dependent cell-mediated cytotoxicity (ADCC), cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM) and they are then recognized by natural killer (NK) cells and macrophages, which in turn kill these tagged cells. Type III hypersensitivity is otherwise known as immune complex hypersensitivity. This type of reaction occurs when there is little antibody and an excess of antigen, leading to the formation of small immune complexes. This reaction usually takes 2-8 hrs to have results. In this case the Ag- Ab complexes are