Allergome-wide peptide microarrays enable epitope deconvolution in allergen-specific immunotherapy.


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:
03 2021
Historique:
received: 11 12 2019
revised: 22 07 2020
accepted: 04 08 2020
pubmed: 14 8 2020
medline: 23 9 2021
entrez: 14 8 2020
Statut: ppublish

Résumé

The interaction of allergens and allergen-specific IgE initiates the allergic cascade after crosslinking of receptors on effector cells. Antibodies of other isotypes may modulate such a reaction. Receptor crosslinking requires binding of antibodies to multiple epitopes on the allergen. Limited information is available on the complexity of the epitope structure of most allergens. We sought to allow description of the complexity of IgE, IgG We generated an allergome-wide microarray comprising 731 allergens in the form of more than 172,000 overlapping 16-mer peptides. Allergen recognition by IgE, IgG Extensive induction of linear peptide-specific Phl p 1- and Bet v 1-specific humoral immunity was demonstrated in subjects undergoing a 3-year-long AIT against grass and birch pollen allergy, respectively. Epitope profiles differed between subjects but were largely established already after 1 year of AIT, suggesting that dominant allergen-specific antibody clones remained as important contributors to humoral immunity following their initial establishment during the early phase of AIT. Complex, subject-specific patterns of allergen isoform and group cross-reactivities in the repertoires were observed, patterns that may indicate different levels of protection against different allergen sources. The study highlights the complexity and subject-specific nature of allergen epitopes recognized following AIT. We envisage that epitope deconvolution will be an important aspect of future efforts to describe and analyze the outcomes of AIT in a personalized manner.

Sections du résumé

BACKGROUND
The interaction of allergens and allergen-specific IgE initiates the allergic cascade after crosslinking of receptors on effector cells. Antibodies of other isotypes may modulate such a reaction. Receptor crosslinking requires binding of antibodies to multiple epitopes on the allergen. Limited information is available on the complexity of the epitope structure of most allergens.
OBJECTIVES
We sought to allow description of the complexity of IgE, IgG
METHODS
We generated an allergome-wide microarray comprising 731 allergens in the form of more than 172,000 overlapping 16-mer peptides. Allergen recognition by IgE, IgG
RESULTS
Extensive induction of linear peptide-specific Phl p 1- and Bet v 1-specific humoral immunity was demonstrated in subjects undergoing a 3-year-long AIT against grass and birch pollen allergy, respectively. Epitope profiles differed between subjects but were largely established already after 1 year of AIT, suggesting that dominant allergen-specific antibody clones remained as important contributors to humoral immunity following their initial establishment during the early phase of AIT. Complex, subject-specific patterns of allergen isoform and group cross-reactivities in the repertoires were observed, patterns that may indicate different levels of protection against different allergen sources.
CONCLUSIONS
The study highlights the complexity and subject-specific nature of allergen epitopes recognized following AIT. We envisage that epitope deconvolution will be an important aspect of future efforts to describe and analyze the outcomes of AIT in a personalized manner.

Identifiants

pubmed: 32791163
pii: S0091-6749(20)31108-8
doi: 10.1016/j.jaci.2020.08.002
pii:
doi:

Substances chimiques

Allergens 0
Antigens, Plant 0
Epitopes, B-Lymphocyte 0
Immunoglobulin Isotypes 0
Peptides 0
Plant Proteins 0
Bet v 1 allergen, Betula 126161-14-6
PHLPI protein, Phleum pratense 160227-82-7
Immunoglobulin E 37341-29-0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1077-1086

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Maria Mikus (M)

Division of Affinity Proteomics, Department of Protein Science, KTH Royal Institute of Technology & SciLifeLab, Stockholm, Sweden; Unit of Experimental Asthma and Allergy Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Arash Zandian (A)

Division of Affinity Proteomics, Department of Protein Science, KTH Royal Institute of Technology & SciLifeLab, Stockholm, Sweden.

Ronald Sjöberg (R)

Division of Affinity Proteomics, Department of Protein Science, KTH Royal Institute of Technology & SciLifeLab, Stockholm, Sweden.

Carl Hamsten (C)

Division of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.

Björn Forsström (B)

Division of Systems Biology, Department of Protein Science, KTH Royal Institute of Technology & SciLifeLab, Stockholm, Sweden.

Morgan Andersson (M)

Department of Otorhinolaryngology, Head & Neck Surgery, Skåne University Hospital, Lund, Sweden.

Lennart Greiff (L)

Department of Otorhinolaryngology, Head & Neck Surgery, Skåne University Hospital, Lund, Sweden; Department of Clinical Sciences, Lund University, Lund, Sweden.

Mathias Uhlén (M)

Division of Systems Biology, Department of Protein Science, KTH Royal Institute of Technology & SciLifeLab, Stockholm, Sweden.

Mattias Levin (M)

Department of Immunotechnology, Lund University, Lund, Sweden.

Peter Nilsson (P)

Division of Affinity Proteomics, Department of Protein Science, KTH Royal Institute of Technology & SciLifeLab, Stockholm, Sweden.

Marianne van Hage (M)

Division of Immunology and Allergy, Department of Medicine Solna, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.

Mats Ohlin (M)

Department of Immunotechnology, Lund University, Lund, Sweden. Electronic address: mats.ohlin@immun.lth.se.

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Classifications MeSH