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Microbiota-dependent crosstalk between macrophages and ILC3 promotes intestinal homeostasis.

ABSTRACT: 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?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?. Our findings reveal that commensal microbes promote a crosstalk between innate myeloid and lymphoid cells that leads to immune homeostasis in the intestine.

SUBMITTER: Mortha A

PROVIDER: S-EPMC4291125 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature

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Microbiota-dependent crosstalk between macrophages and ILC3 promotes intestinal homeostasis.

Mortha Arthur A Chudnovskiy Aleksey A Hashimoto Daigo D Bogunovic Milena M Spencer Sean P SP Belkaid Yasmine Y Merad Miriam M

Science (New York, N.Y.) 20140313 6178

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 RORγt(+) innat ...[more]

PMID: 24625929

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