调节胶质母细胞瘤浸润性骨髓细胞的免疫检查点是一种可行的治疗策略吗?
Is modulation of immune checkpoints on glioblastoma-infiltrating myeloid cells a viable therapeutic strategy?
发表日期:2024 Oct 19
作者:
Ruochen Du, Jianzhong Zhang, Rimas V Lukas, Shashwat Tripathi, Jared T Ahrendsen, Michael A Curran, Crismita Dmello, Peng Zhang, Roger Stupp, Ganesh Rao, Amy B Heimberger
来源:
NEURO-ONCOLOGY
摘要:
免疫学领域传统上专注于适应性免疫细胞的免疫检查点调节。然而,许多恶性肿瘤(例如胶质母细胞瘤)大多缺乏 T 细胞,而是富含先天免疫系统的免疫抑制性骨髓细胞。虽然一些免疫检查点目标在适应性免疫和先天免疫之间共享,但骨髓特异性检查点也可以作为潜在的治疗方法。为了更好地了解免疫检查点阻断对骨髓细胞的影响,我们系统总结了目前关注PD-L1/PD-1、CD24/Siglec-10、胶原蛋白/LAIR-1、CX3CL1/CX3CR1、和 CXCL10/CXCR3。通过综合分子机制和转化意义,我们的目标是优先考虑此类胶质母细胞瘤治疗药物。© 作者 2024。由牛津大学出版社代表神经肿瘤学会出版。版权所有。如需商业重复使用,请联系 reprints@oup.com 获取转载和转载的翻译权。所有其他权限都可以通过我们网站文章页面上的权限链接通过我们的 RightsLink 服务获得 - 如需了解更多信息,请联系journals.permissions@oup.com。
The field of immunology has traditionally focused on immune checkpoint modulation of adaptive immune cells. However, many malignancies such as glioblastoma are mostly devoid of T cells and rather are enriched with immunosuppressive myeloid cells of the innate immune system. While some immune checkpoint targets are shared between adaptive and innate immunity, myeloid-specific checkpoints could also serve as potential therapeutics. To better understand the impact of immune checkpoint blockade on myeloid cells, we systematically summarize the current literature focusing on the direct immunological effects of PD-L1/PD-1, CD24/Siglec-10, collagen/LAIR-1, CX3CL1/CX3CR1, and CXCL10/CXCR3. By synthesizing the molecular mechanisms and the translational implications, we aim to prioritize agents in this category of therapeutics for glioblastoma.© The Author(s) 2024. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.