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Pyruvate enhances oral tolerance via GPR31
Qizhi Liu1,2, Eiji Umemoto1,3, Naoki Morita1,4
1Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, 565-0871, Japan.
International Immunology
|March 18, 2022
Summary
Pyruvate enhances oral tolerance by acting on G-protein coupled receptor 31 (GPR31) on intestinal myeloid cells. This pathway is crucial for inducing regulatory T cells and preventing allergic responses.
Area of Science:
- Immunology
- Gastroenterology
- Microbiome Research
Background:
- Intestinal CX3CR1high myeloid cells drive oral tolerance by promoting regulatory T (Treg) cells.
- Bacterial metabolites like pyruvate and lactate extend myeloid cell dendrites via GPR31.
- The role of the pyruvate-GPR31 axis in oral tolerance remains unclear.
Purpose of the Study:
- To investigate whether the pyruvate-GPR31 axis mediates oral tolerance induction.
- To elucidate the mechanism by which pyruvate influences oral tolerance.
Main Methods:
- Utilized Gpr31-deficient mice and ovalbumin (OVA) feeding to assess oral tolerance.
- Administered pyruvate to wild-type mice and analyzed immune responses.
- Generated CX3CR1high myeloid cell-specific IL-10-deficient mice.
- Quantified Treg cells and measured IL-10 production in the small intestine.
Main Results:
- Pyruvate enhanced oral tolerance in a GPR31-dependent manner.
- Gpr31-deficient mice exhibited defective oral tolerance induction and reduced RORγt+ Treg cells.
- Pyruvate treatment improved oral tolerance in wild-type mice.
- IL-10 production by intestinal myeloid cells was dependent on GPR31.
- Impaired oral tolerance and reduced Treg cell accumulation were observed in IL-10-deficient mice.
Conclusions:
- Pyruvate enhances oral tolerance via a GPR31-dependent mechanism.
- This pathway involves the modulation of intestinal CX3CR1high myeloid cells and IL-10 production.
- The findings highlight a novel role for bacterial metabolites in immune homeostasis.
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