This study investigates the immunomodulatory effects of *Dubosiella newyorkensis*, a murine commensal bacterium, and its human homologue *Clostridium innocuum*, on dextran sulfate sodium-induced colitis in mice. The research identifies that *D. newyorkensis* and *C. innocuum* produce short-chain fatty acids (SCFAs), particularly propionate and L-Lysine (Lys), which help rebalance Treg/Th17 responses and improve mucosal barrier integrity. Lys is shown to induce immune tolerance in dendritic cells (DCs) by enhancing tryptophan (Trp) catabolism towards the kynurenine (Kyn) pathway through activation of indoleamine-2,3-dioxygenase 1 (IDO1) in an aryl hydrocarbon receptor (AhR)-dependent manner. This metabolic pathway, known as the AhR-IDO1-Kyn circuitry, is crucial for establishing a Treg-mediated immunosuppressive microenvironment. The study suggests that this metabolic communication may represent a potential therapeutic target for inflammatory bowel diseases.This study investigates the immunomodulatory effects of *Dubosiella newyorkensis*, a murine commensal bacterium, and its human homologue *Clostridium innocuum*, on dextran sulfate sodium-induced colitis in mice. The research identifies that *D. newyorkensis* and *C. innocuum* produce short-chain fatty acids (SCFAs), particularly propionate and L-Lysine (Lys), which help rebalance Treg/Th17 responses and improve mucosal barrier integrity. Lys is shown to induce immune tolerance in dendritic cells (DCs) by enhancing tryptophan (Trp) catabolism towards the kynurenine (Kyn) pathway through activation of indoleamine-2,3-dioxygenase 1 (IDO1) in an aryl hydrocarbon receptor (AhR)-dependent manner. This metabolic pathway, known as the AhR-IDO1-Kyn circuitry, is crucial for establishing a Treg-mediated immunosuppressive microenvironment. The study suggests that this metabolic communication may represent a potential therapeutic target for inflammatory bowel diseases.