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CD24/Siglec-10 介导的肿瘤细胞免疫逃逸的分子机制。

Molecular Mechanism of Tumor Cell Immune Escape Mediated by CD24/Siglec-10.

机构信息

Department of Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

Front Immunol. 2020 Jul 17;11:1324. doi: 10.3389/fimmu.2020.01324. eCollection 2020.

Abstract

Tumor immune escape is an important part of tumorigenesis and development. Tumor cells can develop a variety of immunosuppressive mechanisms to combat tumor immunity. Exploring tumor cells that escape immune surveillance through the molecular mechanism of related immunosuppression in-depth is helpful to develop the treatment strategies of targeted tumor immune escape. The latest studies show that CD24 on the surface of tumor cells interacts with Siglec-10 on the surface of immune cells to promote the immune escape of tumor cells. It is necessary to comment on the molecular mechanism of inhibiting the activation of immune cells through the interaction between CD24 on tumor cells and Siglec-10 on immune cells, and a treatment strategy of tumors through targeting CD24 on the surface of tumor cells or Siglec-10 on immune cells.

摘要

肿瘤免疫逃逸是肿瘤发生和发展的重要组成部分。肿瘤细胞可以发展出多种免疫抑制机制来对抗肿瘤免疫。深入探讨肿瘤细胞通过相关免疫抑制的分子机制逃避免疫监视,有助于制定靶向肿瘤免疫逃逸的治疗策略。最新研究表明,肿瘤细胞表面的 CD24 与免疫细胞表面的 Siglec-10 相互作用,促进肿瘤细胞的免疫逃逸。有必要对通过肿瘤细胞表面的 CD24 与免疫细胞表面的 Siglec-10 相互作用抑制免疫细胞激活的分子机制进行评论,并通过靶向肿瘤细胞表面的 CD24 或免疫细胞表面的 Siglec-10 制定肿瘤治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff74/7379889/357227cf62f6/fimmu-11-01324-g0001.jpg

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