ArticleCell communication and signaling : CCS2026
SLC1A5-mediated kynurenine metabolism drives AHR-FANCD2 axis to remodel chromatin and induce T cell exhaustion in lung adenocarcinoma.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundKynurenine, a byproduct of tryptophan breakdown, is linked to immune suppression during cancer development. This study explores the involvement of the amino acid transporter solute carrier family 1 member 5 (SLC1A5) in kynurenine-mediated T cell exhaustion in LUAD and delves into its functional mechanism.
methodsRNA-sequencing analysis was employed to identify transcriptome differences between T progenitor and terminal exhausted T cells (TPEX vs. TEX). The SLC1A5 expression was detected in T cells following L-kynurenine (L-ky) treatment. Mouse LUAD cells LLC were implanted into wild-type (WT), SLC1A5 knockout (SLC1A5
resultsSLC1A5 is upregulated in TEX, and its expression in CD8
conclusionThis study suggests that SLC1A5 is upregulated in TEX, which modulates kynurenine metabolism and induces T cell exhaustion through the AHR-FANCD2 axis-mediated chromatin remodeling.
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