Department of Molecular Biosciences, Faculty of Life Sciences, Kyoto Sangyo University, Kita-ku, Kyoto, Japan.
J Biochem. 2019 May 1;165(5):387-390. doi: 10.1093/jb/mvz003.
Aberrant glycosylation on tumour cells has been implicated in tumour immune modulation. A recent article published in The Journal of Biochemistry (Sutoh Yoneyama et al., A mechanism for evasion of CTL immunity by altered O-glycosylation of HLA class I, J. Biochem. 2017;161:479-492) showed that bladder cancer cells evaded cytotoxic T lymphocyte-mediated antitumour immunity by a novel mechanism involving the loss of Core 2 structures on human leukocyte antigen Class I O-glycans and subsequent impairment of galectin-glycan lattice formation. The immunosuppressive action of O-glycans on natural killer cell-mediated tumour immunity is also considered an immune evasion system. Furthermore, sialylated O-glycans have been proposed to play a central role in tumour immune escape by modulating the production of immunoregulatory cytokines and growth factors through interactions with sialic acid-binding immunoglobulin-like lectins. Therefore, a better understanding of how alterations in O-glycosylation influence tumour immune evasion will enable the development of novel and more effective therapeutic options for cancer treatment.
肿瘤细胞上的异常糖基化被认为与肿瘤免疫调节有关。最近发表在《生物化学杂志》上的一篇文章（Sutoh Yoneyama 等人，改变 HLA I 类的 O-糖基化逃避 CTL 免疫的机制，J. Biochem. 2017;161:479-492）表明，膀胱癌细胞通过一种新的机制逃避细胞毒性 T 淋巴细胞介导的抗肿瘤免疫，该机制涉及人类白细胞抗原 I 类 O-聚糖核心 2 结构的丢失，随后影响半乳糖凝集素-聚糖晶格的形成。O-聚糖对自然杀伤细胞介导的肿瘤免疫的免疫抑制作用也被认为是一种免疫逃逸系统。此外，唾液酸化的 O-聚糖通过与唾液酸结合免疫球蛋白样凝集素相互作用，调节免疫调节细胞因子和生长因子的产生，从而在肿瘤免疫逃逸中发挥核心作用。因此，更好地了解 O-糖基化的改变如何影响肿瘤免疫逃逸，将能够为癌症治疗开发新的、更有效的治疗选择。
