SLC1A5-mediated kynurenine metabolism drives AHR-FANCD2 axis to remodel chromatin and induce T cell exhaustion in lung adenocarcinoma | Synapse
February 19, 2026Open Access
SLC1A5-mediated kynurenine metabolism drives AHR-FANCD2 axis to remodel chromatin and induce T cell exhaustion in lung adenocarcinoma
Key Points
The research aims to explore the role of SLC1A5 in kynurenine metabolism and its impact on T cell exhaustion.
Analysis of SLC1A5 expression in T cell exhaustion (TEX) models
Assessment of kynurenine metabolism pathways
Investigation of the AHR-FANCD2 axis
Evaluation of chromatin remodeling effects on T cells
SLC1A5 is significantly upregulated in TEX
Kynurenine metabolism is altered, promoting T cell exhaustion
The AHR-FANCD2 axis is involved in chromatin remodeling
Abstract
This 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.