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Review
. 2016 Jun;137(6):1662-1670.
doi: 10.1016/j.jaci.2016.04.010. Epub 2016 Apr 27.

IgE in the diagnosis and treatment of allergic disease

Affiliations
Review

IgE in the diagnosis and treatment of allergic disease

Thomas A E Platts-Mills et al. J Allergy Clin Immunol. 2016 Jun.

Abstract

Traditionally, the concept of allergy implied an abnormal response to an otherwise benign agent (eg, pollen or food), with an easily identifiable relationship between exposure and disease. However, there are syndromes in which the relationship between exposure to the relevant allergen and the "allergic" disease is not clear. In these cases the presence of specific IgE antibodies can play an important role in identifying the relevant allergen and provide a guide to therapy. Good examples include chronic asthma and exposure to perennial indoor allergens and asthma related to fungal infection. Finally, we are increasingly aware of forms of food allergy in which the relationship between exposure and the disease is delayed by 3 to 6 hours or longer. Three forms of food allergy with distinct clinical features are now well recognized. These are (1) anaphylactic sensitivity to peanut, (2) eosinophilic esophagitis related to cow's milk, and (3) delayed anaphylaxis to red meat. In these syndromes the immunology of the response is dramatically different. Peanut and galactose α-1,3-galactose (alpha-gal) are characterized by high- or very high-titer IgE antibodies for Ara h 2 and alpha-gal, respectively. By contrast, eosinophilic esophagitis is characterized by low levels of IgE specific for milk proteins with high- or very high-titer IgG4 to the same proteins. The recent finding is that patients with alpha-gal syndrome do not have detectable IgG4 to the oligosaccharide. Thus the serum results not only identify relevant antigens but also provide a guide to the nature of the immune response.

Keywords: Asthma; IgE antibodies; IgG(4); allergen particles; alpha-gal; eosinophilic esophagitis.

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Conflict of interest statement

Disclosure of potential conflict of interest: T. A. E. Platts-Mills has received a grant from ThermoFisher/Phadia. E. A. Erwin is employed by Nationwide Children’s Hospital; has received royalties from UpToDate; and has received travel support from the American College of Allergy, Asthma, and Immunology. S. P. Commins has received personal fees from Genentech and UpToDate and has received a grant from the National Institutes of Health. J. A. Woodfolk has received grants from the National Institutes of Health/National Institute of Allergy and Infectious Diseases and the National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases. A. J. Schuyler declares no relevant conflicts of interest.

Figures

FIG 1
FIG 1
Allergens become airborne and are inhaled in the form of particles, which range from 5 to 30 μm in diameter (Table I). The number of allergen molecules free in the air is essentially zero, and none of the source materials are inhaled.
FIG 2
FIG 2
Contrast between natural exposure to airborne allergen (A) and bronchial provocation with nebulized extract (B). Natural exposure is to relatively large particles, which contain a wide range of allergens and adjuvants.
FIG 3
FIG 3
IgE antibodies in patients with EoE compared with those with 2 anaphylaxis syndromes: peanut and alpha-gal. Although IgE to milk, wheat, egg, and soy are common in children with EoE, the titers are generally low or very low.
FIG 4
FIG 4
Contrast between 3 body surfaces that are relevant to the induction and maintenance of immune responses for food allergens: skin (keratinized squamous epithelium), esophagus (nonkeratinized squamous epithelium), and columnar epithelium in the intestines. We recognize that the lymphoid tissues draining the upper airways and mouth are also important for response to food allergens.

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