Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Figure of data supporting cancer immunotherapy by targeting CD94/NKG2A

Read more