Considering that loss of NR2F6 enhances antitumor responses in T cells, especially during immune-checkpoint inhibition [ 29 , 30 ], loss of NR2F6 in NK cells may be significant for tumors that lack potent T cell epitopes or have downregulated MHC-I expression as an escape mechanism, offering a potential avenue for a combinatorial therapeutic intervention.
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Regulation of NK cell development, maturation, and antitumor responses by the nuclear receptor NR2F6.
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