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While these direct endocrine effects form the core biological axis, their metabolic expression is further modulated by higher-order regulatory systems that integrate stress signaling, immune tone, microbial ecology, and behavioral adaptation

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Mechanistic studies reveal that SFN significantly downregulates programmed death-ligand 1 (PD-L1) expression on tumor cells through multiple mechanisms, including direct covalent modification of cysteine residues on STAT1, which inhibits its transcriptional activity and blocks IFN--induced PD-L1 expression (75)