将黑暗转化为光明：一种 Siglec-9 开关

Tumor-associated immune repression dampens the success of T-cell therapy for cancer by a plethora of inhibitory mechanisms including aberrant glycosylation. In this issue, Eisenberg and colleagues show that IFNγ induces hyper-sialylation of cancer cells and that this acts as the "checkpoint" through binding to the inhibitory molecule Siglec-9 on immune cells.

A chimeric Siglec-9 "switch" receptor converts the suppressive signal into a stimulatory signal, thereby restoring T-cell responses in the tumor tissue, which has multiple implications for the use of adoptive cell therapy in cancer. See related article by Eisenberg et al. , p. 1380 (3).