While interpreting our results, we acknowledge certain limitations. Although we used a cross-sectional study design, a longitudinal study following individual patients over time would be valuable in testing causality. Food-allergic patients had an increased prevalence of atopic dermatitis, allergic rhinitis, and asthma as would be expected, and differences in Treg cells may be important in the atopic march process and not solely food allergy. Therefore, some of our findings could have broader implications for the general predisposition of atopy. In summary, we found that young, atopic food-allergic children have lower percentages of strictly defined Treg cells compared with healthy controls of similar age. Moreover, age-related increases in Treg-cell expression of CCR6 were observed in healthy controls but not food-allergic children, which may be important for Treg-cell migration to peripheral sites of inflammation in the maintenance of tolerance. Our study supports the concept that Treg-cell frequency is associated with the maintenance of tolerance in allergy. Benjamin T. Prince, MD, Msci a,b,c Ashley L. Devonshire, MD, MPH a Kristin A. Erickson b Jenna Bergerson, MD a Dalia Fuleihan, BA b Christine Szychlinski, APN a Robert P. Schleimer, PhD b Paul J. Bryce, PhD b Anne Marie Singh, MD a,b From a the Department of Pediatrics, Division of Allergy and Immunology, Ann & Robert H. Lurie Children’s Hospital of Chicago and b the Department of Medicine, Division of Allergy and Immunology, Northwestern Feinberg School of Medicine, Northwestern University, Chicago, Ill; and c the Department of Pediatrics, Division of Allergy and Immunology, Nationwide Children’s Hospital, The Ohio State University, Columbus, Ohio. E-mail: anne-singh@northwestern.edu. Disclosure of potential conflict of interest: B. T. Prince receives grant funding from Northwestern University Allergy-Immunology T32 National Institutes of Health (NIH) training grant. C. Szychlinski receives payment for lectures from the Mylan Speakers Bureau. R. P. Schleimer receives grant support from the NIH; serves as a consultant for Intersect ENT, GlaxoSmithKline, Allakos, Aurasense, Merck, BioMarck, Sanofi, AstraZeneca/Medimmune, Genentech, Ecicure, Inc, and Ostuka, Inc, and holds stock options from Allakos, Aurasense, BioMarck, and Exicure, Inc. P. J. Bryce serves as a consultant for Allakos; is an employee of Northwestern University; receives grant support from the NIH; and received payments for lectures from FOCIS. A. M. Singh receives grant support from the National Institute of Allergy and Infectious Diseases, Glen and Wendy Miller Family Foundation, Melchiorre Family Foundation, Bunning Food Allergy Initiative, and Thrasher Research Fund. The rest of the authors declare that they have no relevant conflicts of interest. REFERENCES 1. Toit Du G, Roberts G, Sayre PH, Bahnson HT, Radulovic S, Santos AF, et al. Ran- domized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med 2015;372:803-13. 2. Bantz SK, Zhu Z, Zheng T. The atopic march: progression from atopic dermatitis to allergic rhinitis and asthma. J Clin Cell Immunol 2014;5. 3. Syed A, Garcia MA, Lyu S-C, Bucayu R, Kohli A, Ishida S, et al. Peanut oral immunotherapy results in increased antigen-induced regulatory T-cell function and hypomethylation of forkhead box protein 3 (FOXP3). J Allergy Clin Immunol 2014;133:500-11. 4. Qamar N, Fishbein AB, Erickson KA, Cai M, Szychlinski C, Bryce PJ, et al. Naturally occurring tolerance acquisition to foods in previously allergic children is characterized by antigen specificity and associated with increased subsets of regulatory T cells. Clin Exp Allergy 2015;45: 1663-72. 5. Liu W, Putnam AL, Xu-Yu Z, Szot GL, Lee MR, Zhu S, et al. CD127 expression inversely correlates with FoxP3 and suppressive function of human CD41 Treg cells. J Exp Med 2006;203:1701-11. 6. 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Available online May 23, 2017. http://dx.doi.org/10.1016/j.jaci.2017.04.039 Molecular diagnostics and lack of clinical allergy in helminth- endemic areas in Indonesia To the Editor: Parasitic helminths and allergens are potent inducers of T H 2 responses that lead to high levels of IgE. 1 Despite the similar immunological profiles of helminth infections and allergic disorders, several cross-sectional and interventional studies have indicated a negative association between helminth infections and skin prick test (SPT) positivity to allergens. 2 In addition to the possible role of immune-regulatory networks induced by chronic helminth infections, cross-reactive IgE to helminths and environmental/food allergens with low biological activity may prevent mast cell degranulation. 3 The allergen that results in the induction of the original allergic responses is the primary sensitizer, whereas others are considered cross-reactive allergens. IgE cross-reactivities can be due to homologous proteins, or to complex N-glycans on plant and invertebrate glycoproteins, known as cross-reactive carbohydrate determinants (CCDs). 4 The characterization of IgE in helminth-endemic areas has largely been based on allergen extracts. IgE against CCD has a very broad spectrum of cross-reactivity across the plant kingdom, invertebrates such as insects (venoms), and even parasites. Importantly, oral challenge with a CCD-bearing allergen in patients with IgE to CCD proved that CCD-specific IgE is of poor biological activity and has limited, if any, clinical relevance. 5 To fully understand the association between helminths and allergies, it is important to characterize IgE reactivity to allergen components at the molecular level. The ImmunoCAP-ISAC microarray has recently been developed with individual purified natural and recombinant inhalant and food allergens. 6 This allows testing for individual molecular IgE recognition profiles, providing comprehensive information about likely sources of primary sensitization and cross-reactivity and helps elucidate the process of sensitizations and identify risk and protective factors for clinical phenotypes. To elucidate the molecular basis of the extremely high prevalence of sensitization to common allergen sources (65% to 85%) among Indonesian school children, living in a helminth-endemic area, who have very low SPT reactivity and virtually absent clinical allergy, the IgE profiles to allergen components on ImmunoCAP-ISAC chips was studied. The study population selection from the ImmunoSPIN (www.immunospin.org) program, 7 and all methods are given in this article’s Online Repository at www.jacionline.org. Of the study subjects, 93% were infected with soil-transmitted J ALLERGY CLIN IMMUNOL OCTOBER 2017 1196 LETTERS TO THE EDITOR