Of tryptophan metabolites altered in CKD, the broadest knowledge on metabolite-immune interaction is present for IS that triggered pro-inflammatory cytokine release from monocytes/macrophages [TNF-α, IL-1β, IL-6, monocyte chemotactic protein 1 (MCP1)] and induced reactive oxygen species (ROS) for which different mechanisms were described, including activation of the aryl hydrocarbon receptor (AhR), induction of Notch and yes-associated protein (YAP) signalling, and β-catenin inhibition [61–63]. This evidence concerns the gene CCL2 and chronic kidney disease.