ALLERGY AND HYPERSENSITIVITY
An important undesirable side effect of immunity is the development, under some conditions, of allergy or other types of immune hypersensitivity. There are several types of allergy and other hypersensitivities, some of which occur only in people who have a spe-cific allergic tendency.
Delayed-reaction allergy is caused by activated T cells and not by antibodies. In the case of poison ivy, the toxin of poison ivy in itself does not cause much harm to the tissues. However, on repeated exposure, it does cause the formation of activated helper and cytotoxic T cells. Then, after subsequent exposure to the poison ivy toxin, within a day or so, the activated T cells diffuse from the circulating blood in large numbers into the skin to respond to the poison ivy toxin. And, at the same time, these T cells elicit a cell-mediated type of immune reaction. Remembering that this type of immunity can cause release of many toxic sub-stances from the activated T cells as well as extensive invasion of the tissues by macrophages along with their subsequent effects, one can well understand that the eventual result of some delayed-reaction allergies can be serious tissue damage. The damage normally occurs in the tissue area where the instigating antigen is present, such as in the skin in the case of poison ivy, or in the lungs to cause lung edema or asthmatic attacks in the case of some airborne antigens.
Some people have an “allergic” tendency. Their aller-gies are called atopic allergies because they are caused by a nonordinary response of the immune system. The allergic tendency is genetically passed from parent to child and is characterized by the presence of large quantities of IgE antibodies in the blood. These anti-bodies are called reagins or sensitizing antibodies to distinguish them from the more common IgG anti-bodies. When an allergen (defined as an antigen that reacts specifically with a specific type of IgE reagin antibody) enters the body, an allergen-reagin reaction lakes place, and a subsequent allergic reaction occurs.
A special characteristic of the IgE antibodies (the reagins) is a strong propensity to attach to mast cells and basophils. Indeed, a single mast cell or basophil can bind as many as half a million molecules of IgE antibodies. Then, when an antigen (an allergen) that has multiple binding sites binds with several IgE anti-bodies that are already attached to a mast cell or basophil, this causes immediate change in the mem-brane of the mast cell or basophil, perhaps resulting from a physical effect of the antibody molecules to contort the cell membrane. At any rate, many of the mast cells and basophils rupture; others release special agents immediately or shortly thereafter, including his-tamine, protease, slow-reacting substance of anaphy-laxis (which is a mixture of toxic leukotrienes),eosinophil chemotactic substance, neutrophil chemo-tactic substance, heparin, and platelet activating factors.These substances cause such effects as dilation of the local blood vessels; attraction of eosinophils and neu-trophils to the reactive site; increased permeability of the capillaries with loss of fluid into the tissues; and contraction of local smooth muscle cells. Therefore, several different tissue responses can occur, depend-ing on the type of tissue in which the allergen-reagin reaction occurs. Among the different types of allergic reactions caused in this manner are the following.
Anaphylaxis. When a specific allergen is injecteddirectly into the circulation, the allergen can react with basophils of the blood and mast cells in the tissues located immediately outside the small blood vessels if the basophils and mast cells have been sensitized by attachment of IgE reagins. Therefore, a widespread allergic reaction occurs throughout the vascular system and closely associated tissues. This is called anaphylaxis. Histamine is released into the circulationand causes body-wide vasodilation as well as increased permeability of the capillaries with resultant marked loss of plasma from the circulation. An occasional person who experiences this reaction dies of circula-tory shock within a few minutes unless treated with epinephrine to oppose the effects of the histamine.
Also released from the activated basophils and mast cells is a mixture of leukotrienes called slow-reactingsubstance of anaphylaxis. These leukotrienes can causespasm of the smooth muscle of the bronchioles, elicit-ing an asthma-like attack, sometimes causing death by suffocation.
Urticaria. Urticaria results from antigen entering spe-cific skin areas and causing localized anaphylactoid reactions. Histamine released locally causes (1) vasodi-lation that induces an immediate red flare and (2) increased local permeability of the capillaries that leads to local circumscribed areas of swelling of the skin within another few minutes. The swellings are commonly called hives.Administration of antihista-mine drugs to a person before exposure will prevent the hives.
Hay Fever. In hay fever, the allergen-reagin reactionoccurs in the nose. Histamine released in response to the reaction causes local intranasal vascular dilation, with resultant increased capillary pressure as well as increased capillary permeability. Both these effects cause rapid fluid leakage into the nasal cavities and into associated deeper tissues of the nose; and the nasal linings become swollen and secretory. Here again, use of antihistamine drugs can prevent this swelling reaction. But other products of the allergen-reagin reaction can still cause irritation of the nose, eliciting the typical sneezing syndrome.
Asthma. Asthma often occurs in the“allergic”type ofperson. In such a person, the allergen-reagin reaction occurs in the bronchioles of the lungs. Here, an impor-tant product released from the mast cells is believed to be the slow-reacting substance of anaphylaxis, which causes spasm of the bronchiolar smooth muscle. Con-sequently, the person has difficulty breathing until the reactive products of the allergic reaction have been removed. Administration of antihistaminics has less effect on the course of asthma because histamine does not appear to be the major factor eliciting the asthmatic reaction.
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