Scientists at Northwestern Medicine have discovered that the immune receptor A2A plays a surprising dual role in cancer. Instead of acting only as an immune “brake,” both excessive A2A activity and its complete loss can push cancer-fighting CD8+ T cells into an exhausted, ineffective state through different biological pathways. Using advanced single-cell analysis, researchers identified CD122 signaling as a key driver of this process when A2A is absent. The findings help explain why A2A-targeted cancer therapies have shown limited success in clinical trials and suggest that future treatments should carefully fine-tune immune signaling rather than simply blocking it, potentially leading to more effective cancer immunotherapies.
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