Interrupting reactivation of immunologic memory diverts the allergic response and prevents anaphylaxis.
Anaphylaxis
/ immunology
Animals
CD4-Positive T-Lymphocytes
/ immunology
Cytokines
/ immunology
Disease Models, Animal
Female
Humans
Immunoglobulin E
/ immunology
Immunologic Memory
Leukocytes, Mononuclear
/ immunology
Mice, Inbred C57BL
Peanut Hypersensitivity
/ immunology
Receptors, Interleukin-4
/ immunology
IL-4 receptor
IgE
T(H)2 immunity
anaphylaxis
food allergy
memory response
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:
04 2021
04 2021
Historique:
received:
01
05
2020
revised:
02
10
2020
accepted:
06
11
2020
pubmed:
19
12
2020
medline:
21
9
2021
entrez:
18
12
2020
Statut:
ppublish
Résumé
IgE production against innocuous food antigens can result in anaphylaxis, a severe life-threatening consequence of allergic reactions. The maintenance of IgE immunity is primarily facilitated by IgG Our aim was to investigate the critical requirements for an IgE recall response in peanut allergy. We used a novel human PBMC culture platform, a mouse model of peanut allergy, and various experimental readouts to assess the IgE recall response in the presence and absence of IL-4Rα blockade. In human PBMCs, we have demonstrated that blockade of IL-4/IL-13 signaling aborted IgE production after activation of a recall response and skewed the cytokine response away from a dominant type 2 signature. T The findings reported here advance our understanding of events mediating the regeneration of IgE in food allergy.
Sections du résumé
BACKGROUND
IgE production against innocuous food antigens can result in anaphylaxis, a severe life-threatening consequence of allergic reactions. The maintenance of IgE immunity is primarily facilitated by IgG
OBJECTIVE
Our aim was to investigate the critical requirements for an IgE recall response in peanut allergy.
METHODS
We used a novel human PBMC culture platform, a mouse model of peanut allergy, and various experimental readouts to assess the IgE recall response in the presence and absence of IL-4Rα blockade.
RESULTS
In human PBMCs, we have demonstrated that blockade of IL-4/IL-13 signaling aborted IgE production after activation of a recall response and skewed the cytokine response away from a dominant type 2 signature. T
CONCLUSION
The findings reported here advance our understanding of events mediating the regeneration of IgE in food allergy.
Identifiants
pubmed: 33338539
pii: S0091-6749(20)31763-2
doi: 10.1016/j.jaci.2020.11.042
pii:
doi:
Substances chimiques
Cytokines
0
Receptors, Interleukin-4
0
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
1381-1392Informations de copyright
Copyright © 2020. Published by Elsevier Inc.