Type I hypersensitivity is characterized by an allergic reaction that occurs immediately following contact with antigen, which is referred to as the allergen. The term allergy means ''changed reactivity'' of the host when meeting an ''agent'' on a second or subsequent occasion. In some individuals certain allergens have a propensity to stimulate production of IgE antibodies. IgE antibodies bind nonspecifically, via their high affinity Fc receptors, to mast cells and basophils. Subsequent attachment of antigen to the Fab portion of cell-bound IgE antibodies results in release of contents of cytoplasmic granules from mast cells and basophils (e.g. histamine), as well as in synthesis and secretion of biologically active products of arachidonic acid (e.g. leukotrienes). Mast cell products increase vascular permeability and constrict bronchial smooth muscle. A wheal and flare reaction occurs within seconds to minutes. Neutrophils and eosinophils characteristically predominate and mononuclear cells can also be seen.
Reaginic reactions are responsible for such allergic phenomena as urticaria, seasonal rhinitis, asthma, and in settings where large amounts of antigens (allergens) enter the host circulation, systemic anaphylaxis. These occur when an IgE response is directed against innocuous enviromental antigens, such as pollen, house-dust mites or animal dander. The resulting release of pharmacological mediators by IgE-sensitized mast cell produces an acute inflammatory reaction with symptoms such as asthma or rhinitis. The importance of type I reactions in protection from infectious organisms is uncertain, although the increased vascular permeability mediated by these reactions probably facilitates the capacity of antibody and inflammatory cells to arrive at the infected site. In addition, homocytotropic IgE antibodies and cells containing inflammatory mediators probably participate in the defence against large, non-phagocytable organisms, most notably the multicellular helminthic parasites.
There is an important question why one individual express atopic diseases and another does not. At least two reasons exist -- environmental exposure and genetics. A third reason -- an external event that alters IgE regulation -- may be important in certain clinical situation but may represent a rare cause of atopic diseases.
The atopic diseases, allergic rhinitis, asthma, and atopic dermatitis have a genetic component. Some or all of these clinical syndromes can be present in a single member or in several member of the same family. The natural history of atopic diseases is not known, but it appears that atopic individuals appear to have a relatively high frequency of food allergy before the age of two years; food allergy then becomes rarer but the patients develop IgE antibodies to inhalant allergens and manifest allergic rhinitis and/or asthma.
In general, atopy is a hereditary feature manifested by abnormal immediated -- type hypersensitivity to a certain allergen or a group of allergens.
Anaphylaxis denotes an acute systemic immediate reaction to allergen, typically mediated by IgE antibodies. The mildest form of anaphylaxis, involving only the skin, is termed urticaria or ''hives''. More severe reactions involve the mucous membranes and the gastrointestinal, pulmonary, and cardiovascular organs. Anaphylaxis may be life-threatening. The manifestations range from urticaria to angioedema (swelling of mucous membranes, for example, of the lips, tongue, palate, and larynx), nausea and vomiting (edema and smooth muscle contraction of gastrointestinal tract), asthma (bronchial smooth muscle contraction), and hypotension (increased vascular permeability resulting in a loss of blood volume into tissue and thus a fall in blood pressure; reducing contractility of the heart also contributes to hypotension). Life-threatening reactions involve laryngeal edema, severe asthma, or severe hypotension and circulatory collapse. Agents that induce IgE-mediated anaphylaxis include penicillin, insect venoms, foods, and occasionally immunotherapy (i.e. injection of allergen to which a person is allergic, in order to treat allergic diseases).
Identical symptoms, which are not immune mediated, are sometimes termed anaphylactoid. Anaphylactoid reactions may be caused by radiocontrast dye (used for x-ray studies) and exercise.
Although antigen-IgE antibody interaction is the major cause of anaphylaxis, other immune mechanisms may occasionally induce the syndrome. Thus immune complexes may mediate anaphylaxis in some patients who are IgA-deficient and receive infusions of IgA, which interacts with preformed anti-IgA antibody. Anaphylactoid reactions may also occur after repeated intravenous administration of normal human immunoglobulin preparation that contain more than 5% of IgG aggregates in agammaglobulinaemic or hypogammaglobulinaemic patients. These aggregates activate complement to produce C5a and C3a anaphylatoxins which stimulate mediator release from basophils and perhaps some subsets of mast cells.