Evolution of epitope-specific IgE and IgG


Journal

The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002

Informations de publication

Date de publication:
09 2021
Historique:
received: 30 07 2020
revised: 15 12 2020
accepted: 15 01 2021
pubmed: 17 2 2021
medline: 11 11 2021
entrez: 16 2 2021
Statut: ppublish

Résumé

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. We sought to compare the evolution of ses-IgE and ses-IgG 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-IgG 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-IgG 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-IgG

Sections du résumé

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-IgG
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-IgG
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-IgG
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-IgG

Identifiants

pubmed: 33592205
pii: S0091-6749(21)00216-5
doi: 10.1016/j.jaci.2021.01.030
pmc: PMC8480440
mid: NIHMS1684849
pii:
doi:

Substances chimiques

Allergens 0
Antigens, Plant 0
Ara h 1 protein, Arachis hypogaea 0
Ara h 3 allergen, Arachis hypogea 0
Epitopes 0
Immunoglobulin G 0
Membrane Proteins 0
Plant Proteins 0
Immunoglobulin E 37341-29-0

Types de publication

Journal Article Randomized Controlled Trial Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

835-842

Subventions

Organisme : NIAID NIH HHS
ID : N01AI15416
Pays : United States
Organisme : NIAID NIH HHS
ID : HHSN272200800029C
Pays : United States
Organisme : NIAID NIH HHS
ID : UM1 AI109565
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM062754
Pays : United States
Organisme : NIAID NIH HHS
ID : UM2 AI117870
Pays : United States

Informations de copyright

Copyright © 2021 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.

Références

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pubmed: 31804555
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pubmed: 29097103
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pubmed: 16210066
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Auteurs

Mayte Suarez-Farinas (M)

Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY; Center for Biostatistics, Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY.

Maria Suprun (M)

Division of Pediatric Allergy and Immunology, Icahn School of Medicine at Mount Sinai, New York, NY.

Henry T Bahnson (HT)

Benaroya Research Institute and the Immune Tolerance Network, Seattle, Wash.

Rohit Raghunathan (R)

Center for Biostatistics, Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY.

Robert Getts (R)

AllerGenis LLC, Hatfield, Pa.

George duToit (G)

Department of Pediatrics, St Thomas Hospital and King's College London, London, United Kingdom.

Gideon Lack (G)

Department of Pediatrics, St Thomas Hospital and King's College London, London, United Kingdom.

Hugh A Sampson (HA)

Division of Pediatric Allergy and Immunology, Icahn School of Medicine at Mount Sinai, New York, NY. Electronic address: hugh.sampson@mssm.edu.

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Classifications MeSH