Magnolia Research Center, Division of Biomedical Sciences, Department of Microbiology and Immunology, Edward Via College of Osteopathic Medicine Carolinas Campus, Spartanburg, SC, 29303, USA.
Department of Biology, Chemistry and Physics, Converse College, Spartanburg, SC, 29302, USA.
Sci Rep. 2019 Oct 10;9(1):14623. doi: 10.1038/s41598-019-51106-y.
No human has returned to the moon since the end of the Apollo program 47 years ago, however, new missions are planned for an orbital outpost. Space radiation and the potential for cancer remain as important issues to the future of human space exploration. While improved shield technologies and protective biologicals are under development, little is known concerning the interaction between cancer cells and host immunity in microgravity. As a hallmark of cancer, tumor cells employ mechanisms of immune evasion to avoid elimination by protective CD4 and CD8 T cells. We showed that a murine lymphoma was able to produce a soluble factor that inhibited the function of dendritic cells in activating the CD4 T cells. Culture of the lymphoma cells in simulated microgravity (SMG), and not Static conditions, restored the CD4 T cell response and augmented CD8 T cell-mediated destruction of the cancer cells in vitro and in vivo. Thus, SMG impaired the mechanism of tumor escape and rendered the cancer cells more susceptible to T cell-mediated elimination. The stress of microgravity may expose the most critical components of a tumor's escape mechanism for astronaut protection and the generation of new cancer therapeutics for patients on Earth.
自 47 年前阿波罗计划结束以来，还没有人返回月球，然而，新的任务计划是在轨道前哨站进行。太空辐射和癌症的潜在风险仍然是人类太空探索未来的重要问题。虽然正在开发改进的屏蔽技术和保护性生物制剂，但对于微重力环境下癌细胞与宿主免疫之间的相互作用知之甚少。作为癌症的一个标志，肿瘤细胞采用免疫逃避机制来避免被保护性 CD4 和 CD8 T 细胞清除。我们发现一种鼠淋巴瘤能够产生一种可溶性因子，抑制树突状细胞激活 CD4 T 细胞的功能。在模拟微重力（SMG）而非静态条件下培养淋巴瘤细胞，恢复了 CD4 T 细胞的反应，并增强了 CD8 T 细胞介导的体外和体内癌细胞的破坏。因此，SMG 破坏了肿瘤逃逸的机制，使癌细胞更容易被 T 细胞介导的清除。微重力的压力可能会暴露肿瘤逃逸机制的最关键部分，以保护宇航员，并为地球上的患者开发新的癌症治疗方法。
