期刊
IMMUNITY
卷 41, 期 1, 页码 141-151出版社
CELL PRESS
DOI: 10.1016/j.immuni.2014.05.017
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类别
资金
- NIH NIAID [R01 AI085090, R56 AI100889, T32 AI007512, P30 DK034854]
- Boston Children's Hospital Translational Research Program
- Rao Chakravorti Family Fund
- Bunning Foundation
Immunoglobulin E (IgE) antibodies are known for triggering immediate hypersensitivity reactions such as food anaphylaxis. In this study, we tested whether they might additionally function to amplify nascent antibody and T helper 2 (Th2) cell-mediated responses to ingested proteins and whether blocking IgE would modify sensitization. By using mice harboring a disinhibited form of the IL-4 receptor, we developed an adjuvant-free model of peanut allergy. Mast cells and IgE were required for induction of antibody and Th2-cell-mediated responses to peanut ingestion and they impaired regulatory T (Treg) cell induction. Mast-cell-targeted genetic deletion of the Fc epsilon RI signaling kinase Syk or Syk blockade also prevented peanut sensitization. In mice with established allergy, Syk blockade facilitated desensitization and induction of Treg cells, which suppressed allergy when transferred to naive recipients. Our study suggests a key role for IgE in driving Th2 cell and IgE responses while suppressing Treg cells in food allergy.
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