西格莱克
免疫系统
免疫检查点
癌细胞
癌症免疫疗法
免疫疗法
受体
生物
癌症研究
细胞生物学
癌症
免疫学
遗传学
出处
期刊:Cancer immunology research
[American Association for Cancer Research]
日期:2024-07-22
卷期号:: OF1-OF1
标识
DOI:10.1158/2326-6066.cir-24-0429
摘要
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).
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