肿瘤微环境对经典霍奇金淋巴瘤检查点抑制剂疗法的影响

IF 0.9 Q4 HEMATOLOGY Hemato Pub Date : 2024-06-03 DOI:10.3390/hemato5020016
A. Gloghini, Antonino Carbone
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引用次数: 0

摘要

经典霍奇金淋巴瘤(cHL)是一种 B 细胞淋巴瘤,其中的肿瘤细胞,即所谓的霍奇金-里德-斯特恩伯格(HRS)细胞,与非恶性细胞类型混杂在一起,而这些细胞是该疾病的功能性组成部分。免疫细胞、成纤维细胞、特化间质细胞和微血管共同构成了肿瘤微环境,并与肿瘤细胞发生功能性相互作用。HRS 细胞周围有 T 细胞和 B 细胞,并混有浆细胞、巨噬细胞、嗜酸性粒细胞和肥大细胞。HRS 细胞与 TME 的免疫细胞之间会发生交叉对话。这种交叉对话由 HRS 细胞表达的大量细胞因子和趋化因子网络或 TME 不同类型细胞产生的分子(即 CD30/CD30L、CD40/CD40L、OX40L/OX40、Il- 3/Il-3R、CCR5/CCL5、CD74 巨噬细胞迁移抑制因子/巨噬细胞和 PD-L1/PD-1)介导。TNF受体家族成员CD30和CD40的过度表达是HRS细胞的一个特征。本综述重点介绍了目前作为免疫检查点阻断手段的新型治疗策略的发展情况,并建议进一步的研究应探索旨在靶向参与癌细胞生长和/或免疫逃逸的 HL 成分的创新分子。希望这将影响个体患者对检查点抑制剂疗法的敏感性或耐药性。
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Tumour Microenvironment Contribution to Checkpoint Inhibitor Therapy in Classic Hodgkin Lymphoma
Classic Hodgkin lymphoma (cHL) is a B-cell lymphoma in which tumour cells, the so-called Hodgkin Reed–Sternberg (HRS) cells, are admixed with non-malignant cell types that are a functional part of the disease. Immune cells, fibroblasts, specialised mesenchymal cells, and microvasculature together make up the tumour microenvironment and have functional interactions with tumour cells. HRS cells are surrounded by T and B cells admixed with plasma cells, macrophages, eosinophils, and mast cells. A cross-talk occurs between HRS cells and immune cells of the TME. This cross-talk is mediated either by a large network of cytokines and chemokines expressed by HRS cells or molecules produced by different cell types of the TME, i.e., CD30/CD30L, CD40/CD40L, OX40L/OX40, Il- 3/Il-3R, CCR5/CCL5, CD74 macrophage migration inhibitory factor/macrophages, and PD-L1/PD-1. The over-expression of CD30 and CD40, members of the TNF receptor family, is a hallmark of HRS cells. This review highlights the current development of newer therapeutic strategies as a means of immune checkpoint blockade and suggests that further research should explore innovative molecules aimed at targeting components of HL that are involved in cancer cell growth and/or immune escape. Hopefully, this will influence sensitivity or resistance to checkpoint inhibitor therapy in an individual patient.
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