Ara h 2 is the dominant peanut allergen despite similarities with Ara h 6 - 05/09/20
Abstract |
Background |
Arachis hypogaea 2 (Ara h 2)-specific IgE is to date the best serologic marker to diagnose peanut allergy. Ara h 6 shares approximately 60% sequence identity and multiple epitopes with Ara h 2.
Objective |
Our aim was to assess the diagnostic utility and relative importance of Ara h 2 and Ara h 6 in peanut allergy.
Methods |
A cohort 100 of children was studied. The cohort included chidren who had peanut allergy, children who were sensitized to but tolerant of peanut, and children who were neither sensitized nor allergic to peanut. Levels of specific IgE to peanut and individual allergens were quantified by using ImmunoCAP. ImmunoCAP inhibition experiments and mast cell activation tests in response to both Ara h 2 and Ara h 6 were performed. Statistical analyses were done using SPSS version 14 and Prism version 7 software.
Results |
Ara h 2–specific IgE and Ara h 6–specific IgE showed the greatest diagnostic accuracy for peanut allergy when compared with specific IgE to peanut and other peanut allergens. Most patients with peanut allergy were sensitized to both Ara h 2 and Ara h 6. Ara h 2 reduced Ara h 2–specific IgE binding more than Ara h 6 did (P < .001), whereas Ara h 6–specific IgE binding was inhibited to a similar degree by Ara h 2 and Ara h 6 (P = .432). In the mast cell activation test, Ara h 2 induced significantly greater maximal reactivity (P = .001) and a lower half maximal effective concentration (P = .002) than did Ara h 6 when testing cosensitized individuals.
Conclusions |
Ara h 2–specific IgE and Ara h 6–specific IgE provide the greatest accuracy to diagnose peanut allergy. Ara h 2 is the dominant conglutin in peanut allergy in the United Kingdom, despite a degree of cross-reactivity with Ara h 6.
Il testo completo di questo articolo è disponibile in PDF.Graphical abstract |
Key words : Ara h 2, Ara h 6, specific IgE, mast cell activation test, ImmunoCAP inhibition, peanut allergy, cross-reactivity
Abbreviations used : AIT, Ara h, EC50, MAT, OFC, ROC, SPT
Mappa
| Supported by the Medical Research Council (Medical Research Council Clinician Scientist Fellowship MR/M008517/1), Asthma UK (grant AUK-BC-2015-01), and the Department of Health via the National Institute for Health Research Comprehensive Biomedical Research Centre Award to Guy's & St. Thomas' NHS Foundation Trust in partnership with King's College London and King’s College Hospital NHS Foundation Trust. |
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| Disclosure of potential conflict of interest: A. F. Santos reports grants and personal fees from the Medical Research Council (grant MR/M008517/1) and grants from Asthma UK and the National Institute of Health Research (NIHR) through a Biomedical Research Centre award to Guy's and St Thomas' NHS Foundation Trust during the conduct of the study, as well as grants from the Immune Tolerance Network/National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health (NIH) and from Asthma UK; personal fees from Thermo Scientific, Nutricia, Infomed, Novartis, Allergy Therapeutics, and Buhlmann; and research support from Buhlmann and Thermo Scientific through a collaboration agreement with King's College London. S. Radulovic reports grants from the NIAID of the NIH, the UK Food Standards Agency (FSA), and the National Peanut Board (NPB). G. Du Toit reports grants from the NIAID of the NIH, Food Allergy & Research Education, the UK Department of Health through the NIHR, the NPB, and UK FSA, all of which partly funded salary over the period of this submitted work. G. Lack reports grants from the NIHR through BRC award to the Guy's and St. Thomas' NHS Foundation Trust, the NPB, the UK FSA, and the Davis Foundation, as well as personal fees from Novartis, Aravax, ALK-Abello, DBV Technologies, and Mighty Mission Me. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 146 - N° 3
P. 621 - Settembre 2020 Ritorno al numero
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