Advertisement
Peanut allergy: a growing phenomenon
Wesley Burks
University of Arkansas for Medical Sciences, Arkansas Children’s Hospital, Little Rock, Arkansas, USA
Address correspondence to: Wesley Burks, Department of Pediatrics, Division of Allergy and Immunology, Arkansas Children’s Hospital, 1120 Marshall Street, Little Rock, Arkansas 72202, USA. Phone: (501) 364-1060; Fax: (501) 364-3173; E-mail: burkswesley@uams.edu.
Find articles by Burks, W. in: JCI | PubMed | Google Scholar
Published April 1, 2003 - More info
J Clin Invest. 2003;111(7):950–952. https://doi.org/10.1172/JCI18233.
© 2003 The American Society for Clinical Investigation
Peanut allergy is one of the most serious of the immediate hypersensitivity reactions to foods in terms of persistence and severity and appears to be a growing problem (1). The prevalence of food hypersensitivity in adults is reportedly less common, but a recent survey in the US found that 1.3% of adults are allergic to peanuts or tree nuts (2). Recently, in a cohort of American children referred for the evaluation of atopic dermatitis, the prevalence of allergic reactivity to peanuts was nearly twice as high as that in a similar group evaluated a decade earlier (3). In spite of increased recognition and understanding of food allergies, food is the single most common cause of anaphylaxis seen in hospital emergency departments (4), accounting for about one-third of anaphylaxis cases seen. It is estimated that about 30,000 food-induced anaphylactic events are seen in American emergency departments each year, 200 of which are fatal (5). Either peanuts or tree nuts cause more than 80% of these reactions.
Due to the persistence of the reaction and the lack of effective treatment, peanut-specific immunotherapy is currently being examined as a treatment option. An understanding of the molecular mechanisms is vital to ensure the eventual, effective treatment of peanut-allergic patients.
-
Th2 polarization of cytokines
The study by Turcanu et al. (6) in this issue of the JCI uses a novel approach, that of CFSE staining to separate peanut-specific lymphocytes by flow cytometry and subsequent cloning. Due to technical difficulties arising from the low frequency of allergen-specific cells in the blood, previous studies have been complicated and not easily interpreted. Human T cells, when repeatedly stimulated in vitro, will often develop a Th2 phenotype regardless of their origin (7, 8).
In this study, the authors compare peanut-allergic individuals, individuals who have outgrown peanut allergy, and those who had always tolerated peanuts (6). Peripheral blood lymphocytes in the peanut-allergic individuals demonstrated a Th2 polarization of cytokine production by peanut-specific cells with low levels of IFN-γ and TNF-α and high levels of IL-4, IL-5, and IL-13. In the individuals who had outgrown their peanut allergy and the nonallergic controls, the cytokines showed a Th1 bias with high levels of IFN-γ and TNF-α and low levels of IL-4, IL-5, and IL-13. An interesting part of the study investigated individuals who were allergic to eggs, using similar laboratory and cloning techniques. As in the peanut-specific cells, the egg-allergic individuals’ peripheral blood lymphocytes had a Th2 skewing of their ovalbumin-specific T cells (Figure 1).
Figure 1Foods enter the gastrointestinal tract and undergo protein digestion and then antigen (Ag) processing. Some Ag enters the blood stream to be distributed at distal sites throughout the body (particularly the skin and respiratory mucosa along with sites in the gastrointestinal mucosa). As the antigen-presenting cell presents Ag to the T cell, specific cytokines are produced. In the peanut-allergic individual, the T cells will secrete increased amounts of IL-4, IL-5, and IL-13, among other mediators, and reduced amounts of IFN-γ and TNF-α when compared to that in an individual who is not allergic to peanuts. The T cell in turn regulates eventual peanut-specific IgE production by B cells. Peanut-specific IgE is attached to mast cells in the gastrointestinal tract, skin, and respiratory tract mucosa. Subsequently, on ingestion of peanuts, in the peanut-allergic individual, the protein is digested and the Ag binds peanut-specific IgE on the mast cell, causing activation of the mast cell with mediator release at the mucosal site. Clinical symptoms ensue.
This evidence that peanut antigens do not in themselves induce a Th2 cytokine response is not surprising, since all food allergy patients share similar clinical symptoms in the skin, gastrointestinal tract, and respiratory tract. The results of the present study (6) will help in the evaluation of future immunomodulatory treatments for food allergy and in studies that examine the natural history of food allergic reactions.
Copyright © 2024 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)