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COI investigators led by Professor Tao Dong published data (Abd Hamid M et al) supporting cancer immunotherapy by targeting CD94/NKG2A, to improve the long-term survivability of effector cells such as CD8+ T cells with better cytotoxic functions following combinatory anti-PD-1 treatment, especially in early stage cancer patients.

This research explores the potential contribution of HLA-E and specifically its receptor CD94/NKG2A on tumor immune evasion, when expressed on tumors compared to adjacent tissue and peripheral blood. We report that epithelial-derived cancer cells, tumor macrophages and importantly CD141+ conventional dendritic cells contributed towards HLA-E enrichment in carcinomas. This enrichment correlated to NKG2a upregulation on CD8+TILs but not on CD4+TILs. Interestingly, CD94/NKG2A is found to be exclusively expressed on PD-1highTILs but lack the intratumoral CD103 expession. The enrichment of CD94/NKG2A on human cancer-specific T cells impairs IL-2 receptor-dependent proliferation and affects the IFNγ-mediated response and anti-tumor cytotoxicity. However, these impaired functions can be recovered following antibody-mediated blockade shown in vitroand ex vivo. Altogether, these data suggest enrichment of HLA-E and CD94/NKG2a interaction can impair the survival of TILs in tumor.

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