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Given that the Th17/IL-17 axis contributes to airway inflammation and disease progression in COPD, and that Trp-Kyn pathway activation (e.g., increased Kyn/Trp ratio) is repeatedly observed in this population, dysregulated gut amino acid, particularly Trp metabolism, may alter the composition and signaling strength of AhR ligands, thereby disrupting Treg/Th17 homeostasis and further amplifying bidirectional interactions between systemic and pulmonary inflammation (Christenson et al., 2019