肿瘤相关的免疫抑制通过包括异常糖基化在内的多种抑制机制阻碍了 T 细胞治疗癌症的成功。在本期中，Eisenberg 及其同事表明，IFNγ 会诱导癌细胞过度唾液酸化，并通过与免疫细胞上的抑制分子 Siglec-9 结合而充当“检查点”。嵌合的 Siglec-9“开关”受体将抑制信号转换为刺激信号，从而恢复肿瘤组织中的 T 细胞反应，这对于癌症中过继细胞疗法的使用具有多重意义。请参阅 Eisenberg 等人的相关文章，第 17 页。 XX (3).©2024 美国癌症研究协会。

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. XX (3).©2024 American Association for Cancer Research.