Allergy and Allergic Diseases
26 January 2001

In allergies, the body's immune system responds defensively to foreign substances, or antigens, that pose no real parasitological threat. Antigens that provoke an allergic reaction include certain foods, antibiotics, vitamins, drugs, vaccines, insect and snake venoms, cosmetics, plant chemicals, pollens, dust, molds, iodine-containing dyes and other chemicals. The normal function of the immune system is to produce proteins, or antibodies, designed to bind to and destroy or neutralize antigens. A major class of antibodies are lymphocytes, a type of white blood cell. B-cell lymphocytes respond to the presumed antigen by changing into proliferating antibody-producing blood-plasma cells. Cytotoxic T-cell lymphocytes interact directly with the bacterial or viral invader, while helper T-cells are involved in the proliferation of the B-cell lymphocytes.

There are different types of allergic reactions. Type 1 reactions, which include hay fever, insect venom allergy, and asthma, involve immunoglobulin E (IgE) antibodies. IgE molecules are bound to mast cells, a type of white blood cells found in loose connective tissue. As the IgE antibodies bind with the presumed antigen, the mast cells release granules of histamine, a hormone that stimulates gastric secretion, constricts the bronchial smooth muscle, and dilates blood vessels -- an orchestrated response to a massive parasite attack. In an allergic attack, these actions of the body's defense system becomes the problem: a runny nose, wheezing, and swelling tissues.

In "Allergy and allergic diseases" (New England Journal of Medicine 344 (4 Jan 01): 30), A.B. Kay of Imperial College School of Medicine in London, UK, presents a review of allergy and allergic diseases, making the following points:

1) The term "allergy" was introduced in 1906 by Clemens P. Pirquet [von Cesenatico] (1874- 1929), who used the term to describe both protective immunity and hypersensitivity reactions, but over time, the term has come to be used exclusively for hypersensitivity reactions. The term "atopy" (from the Greek atopos, meaning out of place) is often used to describe IgE-mediated diseases. Persons with atopy have a hereditary predisposition to produce IgE antibodies against common environmental allergens and have one or more "atopic diseases": allergic rhinitis, asthma, or atopic eczema. Some allergic diseases, such as contact dermatitis and hypersensitivity pneumonitis, develop via IgE-independent mechanisms and can be considered non-atopic allergic conditions.

2) We all inhale aero-allergens derived from pollen, house-dust mites, and cat dander. In general, adults and children without atopy mount a low-grade immune response to these aero-allergens, producing several types of immunoglobulin antibodies, but not IgE antibodies. Persons with atopy, in contrast, have an exaggerated immune response to these aero-allergens, the response characterized by the production of allergen-specific IgE antibodies. Such persons also have elevated serum levels of IgE antibodies and positive reactions to extracts of common aero-allergens in skin-prick tests. The immunopathological hallmark of allergic disease is the infiltration of affected tissue by a specific type (type 2) of T-helper cells. The types of T-helper cells are distinguished on the basis of the types of cytokines (substance that promotes cell growth and cell division) that they produce when activated.

3) In utero, T-cells of the fetus are primed by common environmental allergens that cross the placenta, with the immune response of virtually all newborn infants dominated by type 2 T-helper cells. It has been proposed that during subsequent development the normal (i.e., non-atopic) infant's immune system shifts in favor of a type 1 T-helper cell-mediated response to inhaled allergens, whereas in the potentially atopic infant there is a further increase in type 2 T-helper cells that were primed in utero. The crucial point here is that microbes are probably the chief stimuli of protective type 1 T-helper cell immunity.

4) Kay suggests the marked increase in the prevalence of atopic disease in western Europe, the US, and Australasia during recent years indicates the importance of environmental influences. An informative example is the change in the incidence of seasonal allergic rhinitis and asthma after the reunification of Germany. These disorders were less common in East Germany than in West Germany before reunification, whereas since reunification, the prevalence of atopy and hay fever, but not asthma, has increased among children who spent their early childhood in East Germany. The author suggests this phenomenon raises the possibility that a Western lifestyle accounts for the increase in prevalence. In a clean environment relatively free of bacteria and virus, where antibiotics are frequently used for minor illnesses, children may be deprived of the microbial antigens that stimulate type 1 T-helper cells. The author suggests the results of epidemiological studies support this theory.

See An Adaptationist Account of Allergies.





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