Tumor microenvironment in primary central nervous system lymphoma (PCNSL).

IF 4.4 4区医学 Q2 ONCOLOGY

Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-11-18 DOI:10.1080/15384047.2024.2425131

Qiqi Jin, Haoyun Jiang, Ye Han, Litian Zhang, Cuicui Li, Yurong Zhang, Ye Chai, Pengyun Zeng, Lingling Yue, Chongyang Wu

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引用次数: 0

Abstract

Primary central nervous system lymphoma (PCNSL) is one of the rare lymphomas limited to the central nervous system. With the availability of immunotherapy, the tumor microenvironment (TME) attracts much attention nowadays. However, the systematic studies on the TME of PCNSL are lacking. By reviewing the existing research, we found that the TME of PCNSL is infiltrated with abundant TAMs and TILs, among which cytotoxic T cells (CTLs) and M2-polarized macrophages are principal. However, the counts of immune cells infiltrated in the TME of PCNSL are significantly lower than systemic diffuse large B-cell lymphoma (DLBCL). In addition, PCNSL can attract the infiltration of immunosuppressive cells and the loss of HLA I/II expression, overexpress inhibitory immune checkpoints, and release immunosuppressive cytokines to form an immunosuppressive TME. The immunosuppressive effect of TME in PCNSL is significantly stronger than that in systemic DLBCL. These characteristics of TME highlight the immunosuppression of PCNSL.

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原发性中枢神经系统淋巴瘤（PCNSL）的肿瘤微环境。

原发性中枢神经系统淋巴瘤（PCNSL）是局限于中枢神经系统的罕见淋巴瘤之一。随着免疫疗法的出现，肿瘤微环境（TME）备受关注。然而，关于 PCNSL 肿瘤微环境的系统研究却十分缺乏。通过回顾现有研究，我们发现 PCNSL 的肿瘤微环境中浸润着大量的 TAM 和 TIL，其中细胞毒性 T 细胞（CTL）和 M2 极化巨噬细胞是主要的细胞毒性 T 细胞。不过，PCNSL TME 中浸润的免疫细胞数量明显低于全身性弥漫大 B 细胞淋巴瘤（DLBCL）。此外，PCNSL 还能吸引免疫抑制细胞浸润和 HLA I/II 表达缺失，过度表达抑制性免疫检查点，并释放免疫抑制细胞因子，形成免疫抑制性 TME。PCNSL 中 TME 的免疫抑制作用明显强于全身性 DLBCL。TME的这些特点凸显了PCNSL的免疫抑制作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cancer Biology & Therapy 医学-肿瘤学

CiteScore

7.00

自引率

0.00%

发文量

审稿时长

2.3 months

期刊介绍： Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.