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Blockading the interaction between NKG2A and its ligand HLA‑E removes an important brake from innate and adaptive cytotoxic lymphocytes. This approach holds significant promise for improving outcomes across multiple malignancies where tumors exploit this pathway for immune escape. Ongoing clinical trials will further clarify its therapeutic value in oncology settings.
Disrupts the interaction between HLA-E and NKG2A, enhancing NK cell and CD8+ T cell activity.
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