Journal
CELL HOST & MICROBE
Volume 14, Issue 5, Pages 559-570Publisher
CELL PRESS
DOI: 10.1016/j.chom.2013.10.004
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Funding
- European Research Council (ERC) under the European Union's Seventh Framework Programme
- ERC [281785]
- Swiss National Science Foundation
- Canadian Institute of Health Research
- Ambizione fellowship from the Swiss National Science Foundation
- Genaxen Foundation
- Inselspital
- University of Bern
- European Research Council (ERC) [281785] Funding Source: European Research Council (ERC)
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Microbial exposure following birth profoundly impacts mammalian immune system development. Microbiota alterations are associated with increased incidence of allergic and autoimmune disorders with elevated serum IgE as a hallmark. The previously reported abnormally high serum IgE levels in germfree mice suggests that immunoregulatory signals from microbiota are required to control basal IgE levels. We report that germ-free mice and those with low-diversity microbiota develop elevated serum IgE levels in early life. B cells in neonatal germ-free mice undergo isotype switching to IgE at mucosal sites in a CD4 T-cell- and IL-4-dependent manner. A critical level of microbial diversity following birth is required in order to inhibit IgE induction. Elevated IgE levels in germ-free mice lead to increased mast-cell-surface-bound IgE and exaggerated oral-induced systemic anaphylaxis. Thus, appropriate intestinal microbial stimuli during early life are critical for inducing an immunoregulatory network that protects from induction of IgE at mucosal sites.
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