J Clin Invest. 2019 Dec 2;129(12):5089-5091. doi: 10.1172/JCI133415.
Cancer immunotherapy and its budding effectiveness at improving patient outcomes has revitalized our hope to fight cancer in a logical and safe manner. Immunotherapeutic approaches to reengage the immune system have largely focused on reversing immune checkpoint inhibitor pathways, which suppress the antitumor response. Although these approaches have generated much excitement, they still lack absolute success. Interestingly, newly described host-tumor sugar chains (glycosylations) and glycosylation-binding proteins (lectins) play key roles in evading the immune system to determine cancer progression. In this issue of the JCI, Nambiar et al. used patient head and neck tumors and a mouse model system to investigate the role of galactose-binding lectin 1 (Gal1) in immunotherapy resistance. The authors demonstrated that Gal1 can affect immune checkpoint inhibitor therapy by increasing immune checkpoint molecules and immunosuppressive signaling in the tumor. Notably, these results suggest that targeting a tumor's glycobiological state will improve treatment efficacy.
癌症免疫疗法及其提高患者治疗效果的显著成效，使我们重新燃起了以合乎逻辑且安全的方式抗击癌症的希望。免疫疗法主要集中在逆转免疫检查点抑制剂途径，以重新激活免疫系统，这些途径抑制了抗肿瘤反应。尽管这些方法引起了广泛关注，但它们仍缺乏绝对的成功。有趣的是，新近描述的宿主-肿瘤糖链（糖基化）和糖基化结合蛋白（凝集素）在逃避免疫系统以确定癌症进展方面发挥着关键作用。在本期 JCI 中，Nambiar 等人利用患者的头颈部肿瘤和小鼠模型系统，研究了半乳糖结合凝集素 1（Gal1）在免疫疗法耐药中的作用。作者表明，Gal1 可以通过增加肿瘤中的免疫检查点分子和免疫抑制信号来影响免疫检查点抑制剂治疗。值得注意的是，这些结果表明，靶向肿瘤的糖生物学状态将提高治疗效果。
