# Regulation of IgE responses by B cell receptor signaling

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2021 · $396,250

## Abstract

Project Summary/Abstract
Allergic diseases, including asthma, allergic rhinitis, and food allergy, have been steadily increasing in
incidence and disproportionately affect children. Allergic responses can be triggered rapidly upon exposure to
an allergen that binds to IgE antibodies on mast cells and basophils; these cells then degranulate and release
potent pro-inflammatory mediators. If this response occurs systemically, known as anaphylaxis, it can be life-
threatening. However, despite the importance of IgE in allergic disease, the intrinsic mechanisms that regulate
IgE-expressing B cells remain unclear. Recent technical advances have made it possible to directly detect and
visualize IgE+ B cells in mice, revealing that IgE+ B cells undergo an abortive germinal center phase and are
predisposed to differentiate into short-lived plasma cells. These properties of IgE+ B cells restrain IgE
responses and therefore may help protect against allergy and anaphylaxis in healthy individuals. Recent
studies have demonstrated that the distinct features of mouse IgE+ B cells are largely due to the expression of
the membrane IgE B cell receptor, which has weak, chronic signaling activity compared with other isotypes.
The overall objective of this study is to determine how B cell receptor signaling regulates IgE+ B cell responses
in mice and whether these findings are applicable to human B cells. The specific goals of this study are to 1)
elucidate the mechanisms by which B cell receptor signaling regulates IgE plasma cell responses, 2) to
characterize the role of B cell receptor signaling in the dynamics of IgE+ B cells in germinal centers, and 3) to
determine whether human IgE B cell receptors regulate IgE responses in a similar fashion to mouse IgE B cell
receptors. The results from these studies will help us understand how potent IgE-mediated allergic responses
are controlled at a molecular level.
.

## Key facts

- **NIH application ID:** 10054166
- **Project number:** 5R01AI130470-04
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Christopher David Caballero Allen
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $396,250
- **Award type:** 5
- **Project period:** 2017-11-20 → 2022-10-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10054166

## Citation

> US National Institutes of Health, RePORTER application 10054166, Regulation of IgE responses by B cell receptor signaling (5R01AI130470-04). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10054166. Licensed CC0.

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