Journal
SCIENCE
Volume 349, Issue 6251, Pages 989-993Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aac4263
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Funding
- Institut Pasteur
- Agence Nationale de la Recherche (ANR) [11 BSV3 020 01]
- Fondation de la Recherche Medicale [DEq. 2010318246]
- Fondation Simone e Cino Del Duca from Institut de France
- European Commission [MEXT-CT-2006-042374]
- French government's Investissement d'Avenir program, Laboratoire d'Excellence Integrative Biology of Emerging Infectious Diseases [ANR-10-LABX-62-IBEID]
- European Molecular Biology Organization
- European Union
- Japan Society for the Promotion of Science [15K19129]
- Boehringer Ingelheim
- Grants-in-Aid for Scientific Research [15J09641, 15K19129] Funding Source: KAKEN
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Changes to the symbiotic microbiota early in life, or the absence of it, can lead to exacerbated type 2 immunity and allergic inflammations. Although it is unclear how the microbiota regulates type 2 immunity, it is a strong inducer of proinflammatory T helper 17 (T(H)17) cells and regulatory T cells (T-regs) in the intestine. Here, we report that microbiota-induced T-regs express the nuclear hormone receptor ROR gamma t and differentiate along a pathway that also leads to T(H)17 cells. In the absence of ROR gamma t+ T-regs, T(H)2-driven defense against helminths is more efficient, whereas T(H)2-associated pathology is exacerbated. Thus, the microbiota regulates type 2 responses through the induction of type 3 ROR gamma t+ T-regs and T(H)17 cells and acts as a key factor in balancing immune responses at mucosal surfaces.
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