调节性细胞及其对癌症免疫治疗的影响。
Regulatory cells and the effect of cancer immunotherapy.
发表日期:2023 Feb 04
作者:
María Iglesias-Escudero, Noelia Arias-González, Eva Martínez-Cáceres
来源:
Molecular Cancer
摘要:
多种机制和细胞类型参与免疫反应的调节。其中主要包括调节性T细胞(Tregs)、调节性巨噬细胞(Mregs)、髓系抑制细胞(MDSCs)以及其他调节性细胞类型,例如耐受性树突状细胞(tolDCs)、调节性B细胞(Bregs)和间充质干细胞(MSCs)。这些调节性细胞以其抑制免疫反应的能力而著称,但它们也能抑制抗肿瘤免疫反应。因此,许多调节性细胞浸润到肿瘤组织中与不良预后有关。越来越多的证据表明,消除Tregs会增强抗肿瘤免疫反应。然而,全身性消耗Treg细胞还会同时引起有害的自身免疫反应。此外,由于调节性细胞具有高水平的免疫检查点表达,因此也有望通过阻断这些分子并增强免疫反应来发挥免疫检查点抑制剂的部分作用。这表明免疫疗法不仅通过激活特异性效应T细胞而还可以直接或间接削弱肿瘤组织中调节性细胞的抑制活性。本文旨在汇总我们目前对免疫疗法对不同类型调节性细胞的影响的了解以及这些影响如何有助于免疫疗法的应答。
©2023.作者。
Several mechanisms and cell types are involved in the regulation of the immune response. These include mostly regulatory T cells (Tregs), regulatory macrophages (Mregs), myeloid suppressor cells (MDSCs) and other regulatory cell types such as tolerogenic dendritic cells (tolDCs), regulatory B cells (Bregs), and mesenchymal stem cells (MSCs). These regulatory cells, known for their ability to suppress immune responses, can also suppress the anti-tumor immune response. The infiltration of many regulatory cells into tumor tissues is therefore associated with a poor prognosis. There is growing evidence that elimination of Tregs enhances anti-tumor immune responses. However, the systemic depletion of Treg cells can simultaneously cause deleterious autoimmunity. Furthermore, since regulatory cells are characterized by their high level of expression of immune checkpoints, it is also expected that immune checkpoint inhibitors perform part of their function by blocking these molecules and enhancing the immune response. This indicates that immunotherapy does not only act by activating specific effector T cells but can also directly or indirectly attenuate the suppressive activity of regulatory cells in tumor tissues. This review aims to draw together our current knowledge about the effect of immunotherapy on the various types of regulatory cells, and how these effects may be beneficial in the response to immunotherapy.© 2023. The Author(s).