Inflammatory suppression and cancer-associated bypass of the b 0,+ selenium-utilization program in the human intestine

What To Know

This preprint uses single-cell analyses, enteroid and cell models, proteomics, and cytokine perturbations to describe a redox axis centered on the b0,+ transporter (SLC3A1/SLC7A9) and downstream selenoproteins.

In adult Crohn's disease samples the authors observed loss of b0,+-high mature enterocytes and selective reduction of GPX4, which the authors interpret as priming the epithelium for ferroptosis. In contrast, colorectal cancer samples showed low b0,+ with induction of an xCT/thiol antioxidant program consistent with ferroptosis resistance.

The authors note the baseline axis state correlated with anti-TNF response in an exploratory analysis, suggesting potential relevance to therapy response and disease vulnerability, but this is hypothesis-generating rather than a clinical finding.