Proteasome inhibition promotes Foxn1 expression in thymic epithelial cells and induces thymic regeneration in mice - PubMed

6 hours ago

Proteasome inhibition upregulates Foxn1 expression in thymic epithelial cells (TECs) in both mice and humans.
Nitazoxanide (NTZ), an antiparasitic drug, acts as a proteasome inhibitor that induces Foxn1 while maintaining cell viability.
Mechanistically, NTZ triggers endoplasmic reticulum stress and the unfolded protein response, leading to autophagy as a compensatory survival mechanism.
In mice, NTZ treatment accelerates thymic recovery after radiation damage, restoring architecture and cellularity without affecting T-cell selection or tolerance.
The findings position NTZ as a potential therapy for immune deficiencies caused by cancer treatment, infections, or aging-related thymic atrophy.

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