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In vivo and in vitro experiments clarify the hierarchical regulatory mechanisms: Butyrate directly regulates Th17/Treg homeostasis, promotes Treg differentiation through the HDAC1/FoxP3 pathway, and simultaneously inhibits Th17 activation and the expression of IL-17, IL-23, and RORt ( CB indirectly assists immune tolerance by upregulating retinol metabolism, reducing pro-inflammatory microbiota ( Focus on FP: Clostridium mixtures ( FP , Bacteroides faecis, Roseburia intestinalis) restore the Treg/Th17 balance in DSS-induced UC mice, increase IL-10 and IL-4 secretion, reduce pro-inflammatory factors such as TNF, IL-1, and IL-17, and repair the intestinal barrier ( FP cell-free supernatant exerts non-butyrate-dependent anti-inflammatory effects by reducing colonic TNF-/IL-12 and increasing serum IL-10

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The project described was supported in part by the National Center for Advancing Translational Sciences, National Institutes of Health, through Grant 1UL1TR002014-01

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