The prostacyclin receptor PTGIR is a NRF2-dependent regulator of CD8+ T cell exhaustion



Summary

Research indicates that the prostacyclin receptor, PTGIR, plays a crucial role in regulating CD8+ T cell exhaustion, a state of dysfunction that hinders effective immune responses against chronic infections and cancer. The study highlights that PTGIR expression in CD8+ T cells is dependent on NRF2, a transcription factor involved in cellular stress response. Specifically, NRF2 activates PTGIR expression. Loss of PTGIR leads to exacerbated T cell exhaustion, suggesting PTGIR acts as a protective mechanism. These findings identify PTGIR as a potential therapeutic target to improve CD8+ T cell function and enhance anti-tumor immunity by modulating the NRF2-PTGIR axis.

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