关键词: 18F-FDG Glycolysis PD-1/PD-L1 axis PET/CT Radiotherapy

Mesh : Humans B7-H1 Antigen / metabolism Fluorodeoxyglucose F18 Glucose / metabolism Neoplasms / diagnostic imaging radiotherapy Positron Emission Tomography Computed Tomography Programmed Cell Death 1 Receptor Tumor Microenvironment

来  源:   DOI:10.1007/s11604-023-01507-x

Abstract:
Upregulation of PD-1/PD-L1 allows cancer cells to escape from host immune systems by functionally inactivating T-cell immune surveillance. Clinical blockade strategies have resulted in an increased prevalence of patients with late-stage cancers. However, many cancer patients had limited or no response to current immunotherapeutic strategies. Therefore, how to improve the sensitivity of immunotherapy has become the focus of attention of many scholars. Radiotherapy plays a role in the recruitment of T cells in the tumor microenvironment, increases CD4 + and CD8 + T cells, and increases PD-L1 expression, resulting in the synergistically enhanced antitumor effect of irradiation and PD-L1 blockade. Radiotherapy can cause changes in tumor metabolism, especially glucose metabolism. Tumor glycolysis and tumor immune evasion are interdependent, glycolytic activity enhances PD-L1 expression on tumor cells and thus promotes anti-PD-L1 immunotherapy response. Therefore, the mechanism of radiotherapy affecting tumor immunity may be partly through intervention of tumor glucose metabolism. Furthermore, some authors had found that the uptake of 2\'-deoxy-2\'-[18F]fluoro-D-glucose(18F-FDG) was correlated with PD-1/PD-L1 expression. Positron emission tomography/computed tomography (PET/CT) is a non-invasive detection method for PD-1/PD-L1 expression and has several potential advantages over immunohistochemical (IHC), PET/CT can dynamically reflect the expression of PD-1/PD-L1 inside the tumor and further guide clinical treatment.
摘要:
PD-1/PD-L1的上调允许癌细胞通过功能性失活T细胞免疫监视而从宿主免疫系统逃脱。临床阻断策略导致晚期癌症患者的患病率增加。然而,许多癌症患者对目前的免疫治疗策略反应有限或无反应.因此,如何提高免疫治疗的敏感性成为众多学者关注的焦点。放射治疗在肿瘤微环境中招募T细胞中起作用,增加CD4+和CD8+T细胞,并增加PD-L1表达,导致辐射和PD-L1阻断的协同增强的抗肿瘤作用。放疗可以引起肿瘤代谢的改变,尤其是葡萄糖代谢.肿瘤糖酵解和肿瘤免疫逃避是相互依存的,糖酵解活性增强肿瘤细胞上的PD-L1表达,从而促进抗PD-L1免疫疗法反应。因此,放疗影响肿瘤免疫的机制可能部分是通过对肿瘤糖代谢的干预。此外,一些作者发现2'-脱氧-2'-[18F]氟-D-葡萄糖(18F-FDG)的摄取与PD-1/PD-L1表达相关。正电子发射断层扫描/计算机断层扫描(PET/CT)是一种非侵入性的PD-1/PD-L1表达检测方法,与免疫组织化学(IHC)相比具有若干潜在优势,PET/CT可动态反映肿瘤内PD-1/PD-L1的表达情况,进一步指导临床治疗。
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