JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY | 卷:148 |
Evolution of epitope-specific IgE and IgG4 antibodies in children enrolled in the LEAP trial | |
Article | |
Suarez-Farinas, Mayte1,2  Suprun, Maria3  Bahnson, Henry T.5,6  Raghunathan, Rohit2,4  Getts, Robert4  duToit, George7,8  Lack, Gideon7,8  Sampson, Hugh A.3  | |
[1] Icahn Inst Genom & Multiscale Biol, New York, NY 10029 USA | |
[2] Icahn Sch Med Mt Sinai, Ctr Biostat, Dept Populat Hlth Sci & Policy, New York, NY 10029 USA | |
[3] Icahn Sch Med Mt Sinai, Div Pediat Allergy & Immunol, 1425 Madison Ave, New York, NY 10029 USA | |
[4] AllerGenis LLC, Hatfield, Herts, England | |
[5] Benaroya Res Inst, Seattle, WA USA | |
[6] Immune Tolerance Network, Seattle, WA USA | |
[7] St Thomas Hosp, Dept Pediat, London, England | |
[8] Kings Coll London, London, England | |
关键词: Peanut allergy; biomarkers; sequential epitope; antibody; IgE; IgG(4); bead-based epitope assay; | |
DOI : 10.1016/j.jaci.2021.01.030 | |
来源: Elsevier | |
【 摘 要 】
Background: In the LEAP (Learning Early About Peanut Allergy) trial, early consumption of peanut in high-risk infants was found to decrease the rate of peanut allergy at 5 years of age. Sequential epitope-specific (ses-)IgE is a promising biomarker of clinical peanut reactivity. Objective: We sought to compare the evolution of ses-IgE and ses-IgG4 in children who developed (or not) peanut allergy and to evaluate the immunomodulatory effects of early peanut consumption on these antibodies. Methods: Sera from 341 children (LEAP cohort) were assayed at baseline, 1, 2.5, and 5 years of age, with allergy status determined by oral food challenge at 5 years. A bead-based epitope assay was used to quantitate ses-IgE and ses-IgG4 to 64 sequential epitopes fromAra h 1 to Ara h 3 and was analyzed using linear mixed-effect models. Results: In children avoiding peanut who became peanut allergic, the bulk of peanut ses-IgE did not develop until after 2.5 years. Minimal increases of ses-IgE occurred after 1 year in consumers, but not to the same epitopes as those in children developing peanut allergy. No major changes in ses-IgE were seen in nonallergic or sensitized children. IgE in sensitized consumers was detected against peanut proteins. ses-IgG4 increased over time in most children regardless of consumption or allergy status. Conclusions: Early peanut consumption in infants at high risk of developing peanut allergy appears to divert the immunologic response to a presumably protective'' effect. In general, consumers tend to generate ses-IgG4 earlier and in greater quantities than nonconsumers do, whereas only avoiders tend to generate significant quantities of ses-IgE.
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