Th17 cells require the DNA repair sensor xeroderma pigmentosum complementation Group C to control oxidative DNA damage in a murine model - PubMed
17 hours ago
- #Oxidative Stress
- #Th17 Cells
- #DNA Repair
- Th17 cells rely on the DNA repair sensor XPC (Xeroderma Pigmentosum Complementation Group C) to maintain genomic stability and metabolic fitness during differentiation.
- Loss of XPC in a murine model leads to reduced IL-17 production, increased mitochondrial ROS, and heightened oxidative DNA damage, altering metabolic programs.
- XPC interacts with the base excision repair enzyme 8-oxoguanine DNA glycosylase; its absence disrupts coordination between DNA repair pathways, enhancing oxidative lesion incision activity.
- Restoring antioxidant capacity rescues cytokine production and reduces DNA damage in XPC-deficient cells, highlighting its role in redox control.
- XPC is identified as a key coordinator of DNA repair and redox regulation essential for Th17 cell function in inflammatory contexts.