ArticleCell reports2022
Development of allergen-specific IgE in a food-allergy model requires precisely timed B cell stimulation and is inhibited by Fgl2.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Context-dependent regulation of mast cell-mediated food allergy in C57BL/6J mice.The Journal of allergy and clinical immunology · 2026Article
- Multiple roads to IgE memory: A pluralistic model of IgE immunity.Cell reports · 2026Review
- Mechanisms of IgE-mediated food allergy and the role of allergen-specific B cells.FEBS letters · 2026Review
- Perioperative anaphylaxis attributed to acetaminophen following intravenous acetaminophen administration: a case report.JA clinical reports · 2025Article
- T follicular regulatory cells in food allergy promote IgE via IL-4.JCI insight · 2024Article
- Whence and wherefore IgE?Immunological reviews · 2024Review
- Melatonergic Signaling Sustains Food Allergy Through FcεRI Recycling.Research (Washington, D.C.) · 2024Article
- Regulatory T cells in allergic inflammation.Seminars in immunology · 2023Review
- Recent insights into the mechanisms of anaphylaxis.Current opinion in immunology · 2023Review
- Evidence that High-Affinity IgE Can Develop in the Germinal Center in the Absence of an IgG1-Switched Intermediate.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Preclinical evaluation of alternatives to oral immunotherapy for food allergies.Frontiers in allergy · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Immunoglobulin E (IgE) responses are a central feature of allergic disease. Using a well-established food-allergy model in mice, we show that two sensitizations with cognate B cell antigen (Ag) and adjuvant 7 days apart promotes optimal development of IgE+ germinal center (GC) B cells and high-affinity IgE production. Intervals of 3 or 14 days between Ag sensitizations lead to loss of IgE+ GC B cells and an undetectable IgE response. The immunosuppressive factors Fgl2 and CD39 are down-regulated in T follicular helper (TFH) cells under optimal IgE-sensitization conditions. Deletion of Fgl2 in TFH and T follicular regulatory (TFR) cells, but not from TFR cells alone, increase Ag-specific IgE levels and IgE-mediated anaphylactic responses. Overall, we find that Ag-specific IgE responses require precisely timed stimulation of IgE+ GC B cells by Ag. Furthermore, we show that Fgl2 is expressed by TFH cells and represses IgE. This work has implications for the development and treatment of food allergies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.