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The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne

Review Articles

Advances in Immunology
I A N R . M A C K A Y , M. D . , A N D F R E D S . R O S E N , M .D ., Ed i t ors




First of Two Parts
A.B. KAY, M.D., PH.D.

LLERGIC rhinitis, asthma, and atopic eczema are among the commonest causes of chronic ill health. These diseases are increasingin prevalence, and they add considerably to the burden of health care costs. In Sweden, for example, the number of children with allergic rhinitis, asthma, or eczema roughly doubled over a 12-year period,1 and in the United States the annual cost of treating asthma is about $6 billion.2 The term “allergy” was introduced in 1906 by von Pirquet, who recognized that in both protective immunity andhypersensitivity reactions, antigens had induced changes in reactivity.3 With the passage of time the word has become corrupted and is now frequently used synonymously with IgE-mediated allergic disease. It was von Pirquet’s intent that the term should apply to the “uncommitted” biologic response, which may lead either to immunity (a beneficial effect) or allergic disease (a harmful effect). 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 (i.e., allergic rhinitis, asthma, and atopic eczema). Some allergic diseases, such as contact dermatitis and hypersensitivity pneumonitis,develop through IgE-independent mechanisms and in this sense can be considered nonatopic allergic conditions. This article reviews the basis of atopic allergy, the diseases with which it is associated, and approaches to treatment.


and children without atopy mount a low-grade immunologic response; they produce allergen-specific IgG1 and IgG4 antibodies,4 and invitro their T cells respond to the allergen with a moderate degree of proliferation and the production of interferon-g by type 1 helper T (Th1) cells.5-7 Persons with atopy, by contrast, have an exaggerated response characterized by the production of allergen-specific IgE antibodies; they have elevated serum levels of IgE antibodies and positive reactions to extracts of common aeroallergens onskin-prick tests. T cells from their blood respond to allergens in vitro by inducing cytokines produced by type 2 helper T (Th2) cells (i.e., interleukin-4, 5, and 13),5,7 rather than cytokines produced by Th1 cells (interferon-g and interleukin-2). There are many exceptions to this rule, but the immunopathological hallmark of allergic disease is the infiltration of affected tissue by Th2 cells.8-10In utero, T cells of the fetus are primed by common environmental allergens that cross the placenta. As a result, the immune response of virtually all newborn infants is dominated by Th2 cells.11 It has been proposed that during subsequent development the normal (i.e., nonatopic) infant’s immune system shifts in favor of a Th1-mediated response to inhaled allergens (a process termed “immunedeviation”),12 whereas in the potentially atopic infant there is a further increase in Th2 cells that were primed in utero. Microbes are probably the chief stimuli of protective Th1-mediated immunity. Macrophages that engulf microbes secrete interleukin-12, which induces Th1 cells and natural killer cells to produce interferon-g, thereby shifting the immune system into an “allergyprotective”Th1-mediated response. Other factors may also influence whether Th1 or Th2 cells dominate the response, including the amount of allergen, the duration of exposure to the allergen, and the avidity of allergen-specific interactions between T cells and antigen-presenting cells13,14 (Fig. 1).

All of us inhale aeroallergens derived from pollen, house-dust mites, and cat...
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