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3 powder kegs that will be fired upon the interaction of aller- gen with its corresponding cell surface-bound IgE antibody. Understandably, such a reaction proceeds quite rapidly in a sensitized individual following renewed contact with allergen. For example, within minutes, hay fever patients develop symp- toms after inhaling grass pollen, as do individuals allergic to bee venom after being stung. Generally, individuals possessing a genetic predisposition to atopic diseases are extremely prone to develop IgE antibodies to a variety of inhaled or ingested al- lergens. The IgE antibodies may also bind, although with lesser affinity, to some mononuclear cells and in particular to Langer- hans cells in the skin. This phenomenon may be involved in the mechanism of some eczematous skin lesions, including atopic dermatitis (Fig. 3). IgG or IgM antibodies The production of IgG or IgM antibodies requires, as a rule, more massive exposure to allergens than that leading to the formation of IgE antibodies. Upon renewed contact with suf- ficient amounts of allergen, immune complexes may form with serum antibodies and be deposited in various tissues, where they cause an acute inflammatory reaction. Preferential sites for such reactions, depending on the mode of entry and distribu- tion of the allergen, are alveolar walls of the lungs, glomeruli of kidneys, synovial membranes of joints, and walls of small blood vessels of the skin. Sensitized lymphocytes Sensitized lymphocytes are responsible for the clinical mani- festations of so-called delayed hypersensitivity. If an individual has been exposed to allergen and has developed sensitized lymphocytes that are capable of reacting with it, renewed exposure will trigger the lymphocytes to produce an array of glycoproteins, which are called lymphokines. Lymphokines are also mediators capable of causing considerable inflammation in the surrounding tissues, and they have amplifying effects. For example, they stimulate, indiscriminately, other cell types (including macrophages and monocytes), attract these cells to the site of the reaction, and cause the formation of an inflam- matory infiltrate. In the skin, such a reaction manifests itself by redness, swelling, and the formation of an inflammatory papule. Skin reactions occurring upon contact with sensitizing agents (for example, poison ivy and industrial chemicals) also are caused by the same immune mechanism. Because produc- tion of lymphokines by lymphocytes following stimulation by allergens takes several hours and because the reaction becomes clinically apparent only when minimal numbers of infiltrating cells (mostly monocytes) have accumulated at the reaction site, the time elapsed between allergen contact and clinical reaction is usually 24 to 72 hours. Such reactions are therefore termed delayed reactions. Clinical forms and types The clinical manifestations of allergy include allergic rhini- tis (hay fever), bronchial asthma, hives, atopic (endogenous) eczema (atopic dermatitis) and other eczematous skin lesions, and anaphylactic shock. Notably, allergic reactions occur in response to certain foods; they also can result from exposure to certain chemicals and other substances often found in the workplace. Allergy (continued) + ward ' s science + ward ' s science Fig. 3: Atopic dermatitis (eczema) on a man's hand as the result of a severe allergic reaction to latex. (Credit: B. W. Folsom/Shutterstock) Fig. 2: Scanning electron micrograph of western ragweed pollen grains. Credit: BSIP SA/Alamy Stock Photo)