Journal
SCIENCE
Volume 343, Issue 6178, Pages 1477-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1249288
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Funding
- NIH [R01 CA154947A, R01 CA173861, U01 AI095611]
- German Research Foundation (DFG) [MO2380/1-1]
- Division of Intramural Research of the National Institute of Allergy and Infectious Diseases
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The intestinal microbiota and tissue-resident myeloid cells promote immune responses that maintain intestinal homeostasis in the host. However, the cellular cues that translate microbial signals into intestinal homeostasis remain unclear. Here, we show that deficient granulocyte-macrophage colony-stimulating factor (GM-CSF) production altered mononuclear phagocyte effector functions and led to reduced regulatory T cell (T-reg) numbers and impaired oral tolerance. We observed that ROR gamma t(+) innate lymphoid cells (ILCs) are the primary source of GM-CSF in the gut and that ILC-driven GM-CSF production was dependent on the ability of macrophages to sense microbial signals and produce interleukin-1 beta. Our findings reveal that commensal microbes promote a crosstalk between innate myeloid and lymphoid cells that leads to immune homeostasis in the intestine.
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