Epicutaneous allergen immunotherapy induces a profound and selective modulation in skin dendritic-cell subsets.

Food allergy T-cell responses allergen immunotherapy desensitization epicutaneous immunotherapy skin dendritic cells

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:
Nov 2022
Historique:
received: 21 12 2021
revised: 03 05 2022
accepted: 24 05 2022
pubmed: 3 7 2022
medline: 9 11 2022
entrez: 2 7 2022
Statut: ppublish

Résumé

Epicutaneous immunotherapy (EPIT) protocols have recently been developed to restore tolerance in patients with food allergy. The mechanisms by which EPIT protocols promote desensitization rely on a profound immune deviation of pathogenic T- and B-cell responses. To date, little is known about the contribution of skin dendritic cells (skDCs) to T-cell remodeling and EPIT efficacy. We capitalized on a preclinical model of food allergy to ovalbumin (OVA) to characterize the phenotype and functions of OVA Our results showed that both Langerhans cells and dermal conventional cDC1 and cDC2 subsets retained their ability to capture OVA in the skin and to migrate toward the skin-draining lymph nodes during EPIT. However, their activation/maturation status was significantly impaired, as evidenced by the gradual and selective reduction of CD86, CD40, and OVA protein expression in respective subsets. Phenotypic changes during EPIT were also characterized by a progressive diversification of single-cell gene signatures within each DC subset. Interestingly, we observed that OVA Our results therefore emphasize that the acquisition of distinct phenotypic and functional specializations by skDCs during EPIT is at the cornerstone of the desensitization process.

Sections du résumé

BACKGROUND
Epicutaneous immunotherapy (EPIT) protocols have recently been developed to restore tolerance in patients with food allergy. The mechanisms by which EPIT protocols promote desensitization rely on a profound immune deviation of pathogenic T- and B-cell responses.
OBJECTIVE
To date, little is known about the contribution of skin dendritic cells (skDCs) to T-cell remodeling and EPIT efficacy.
METHODS
We capitalized on a preclinical model of food allergy to ovalbumin (OVA) to characterize the phenotype and functions of OVA
RESULTS
Our results showed that both Langerhans cells and dermal conventional cDC1 and cDC2 subsets retained their ability to capture OVA in the skin and to migrate toward the skin-draining lymph nodes during EPIT. However, their activation/maturation status was significantly impaired, as evidenced by the gradual and selective reduction of CD86, CD40, and OVA protein expression in respective subsets. Phenotypic changes during EPIT were also characterized by a progressive diversification of single-cell gene signatures within each DC subset. Interestingly, we observed that OVA
CONCLUSIONS
Our results therefore emphasize that the acquisition of distinct phenotypic and functional specializations by skDCs during EPIT is at the cornerstone of the desensitization process.

Identifiants

pubmed: 35779666
pii: S0091-6749(22)00884-3
doi: 10.1016/j.jaci.2022.05.025
pii:
doi:

Substances chimiques

Ovalbumin 9006-59-1
Allergens 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1194-1208

Informations de copyright

Copyright © 2022 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.

Auteurs

Léo Laoubi (L)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France; DBV Technologies, Montrouge, France.

Morgane Lacoffrette (M)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Séverine Valsesia (S)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Vanina Lenief (V)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Aurélie Guironnet-Paquet (A)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Amandine Mosnier (A)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Gwendoline Dubois (G)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Anna Cartier (A)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Laurine Monti (L)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Jacqueline Marvel (J)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France.

Eric Espinosa (E)

Inserm, U1037, Centre de Recherche en Cancérologie de Toulouse (CRCT), Toulouse, France; Université de Toulouse, Université Paul Sabatier, Toulouse, France.

Bernard Malissen (B)

Centre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS, Marseille, France.

Sandrine Henri (S)

Centre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS, Marseille, France.

Lucie Mondoulet (L)

DBV Technologies, Montrouge, France.

Hugh A Sampson (HA)

DBV Technologies, Montrouge, France; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY.

Audrey Nosbaum (A)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France; Allergology and Clinical Immunology Department, Lyon Sud University Hospital, Pierre Bénite, France.

Jean-François Nicolas (JF)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France; Allergology and Clinical Immunology Department, Lyon Sud University Hospital, Pierre Bénite, France.

Vincent Dioszeghy (V)

DBV Technologies, Montrouge, France.

Marc Vocanson (M)

CIRI-Centre International de Recherche en Infectiologie, Lyon, France; INSERM, U1111, Lyon, France; University of Lyon, Lyon, France; Université de Lyon 1, Lyon, France; Ecole Normale Supérieure de Lyon, Lyon, France; CNRS, UMR 5308, Lyon, France. Electronic address: marc.vocanson@inserm.fr.

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