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How to kill Treg cells for immunotherapy

机译：如何杀死Treg细胞免疫治疗

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Regulatory T cells (Treg cells), which are CD4+ T cells with high expression of the a-chain of the cytokine IL-2 receptor CD25 (ref. 1), restrain inflammation to prevent autoimmune disease but can also stifle vital pro-inflammatory responses. A single injection of PC61, a monoclonal antibody to mouse CD25, into tumor-bearing mice depletes the mice of peripheral CD25+ cells and enhances tumor killing, which establishes the pro-tumorigenic role of Treg cells in cancer. Since that discovery, a high ratio of Treg cells to effector T cells (Teff cells) in the tumor microenvironment (TME) has emerged as a harbinger of poor oncological prognosis. Therefore, depletion of Treg cells within the human TME is postulated to tip the immunological balance in favor of a pro-inflammatory environment and tumor clearance. Unfortunately, there is no unique cell-surface marker that distinguishes Treg cells from Teff cells and would allow selective depletion of Treg cells. However, CD25 is expressed constitutively at high levels on Treg cells but only transiently at lower levels on Teff cells, which might provide a therapeutic window for antibodies targeting these molecules to eliminate intratumoral Treg cells but not Teff cells. In this issue of Nature Cancer, Quezada and colleagues describe an antibody that binds CD25 but does not block pro-inflammatory IL-2 signaling, which improves Teff cell function in the context of the depletion of Treg cells. Initial clinical trials targeting CD25 to selectively achieve depletion of Treg cells used a humanized monoclonal antibody to CD25, daclizumab, previously approved by the US Food and Drug Administration, that was originally developed to dampen the immune response involved in allograft rejection.
机译：调节性T细胞(Treg细胞),CD4 + T细胞高表达的连锁细胞因子受体- 2 CD25 (ref。1),抑制防止炎症免疫性疾病还可以抑制炎性反应至关重要。一个注入PC61,单克隆抗体鼠标CD25、到肿瘤小鼠耗尽外围CD25 +细胞的小鼠和增强建立肿瘤死亡pro-tumorigenic Treg细胞癌症的作用。自发现以来,Treg细胞的比例高效应T细胞在肿瘤(画眉草细胞)微环境(时差)已经成为一个预兆的肿瘤预后差。在人类身上Treg细胞的损耗提示免疫平衡的假设的炎性环境和肿瘤间隙。细胞表面标记区分Treg细胞从画眉草细胞和将允许选择性Treg细胞的损耗。表达了Treg持续在高水平下级细胞只是暂时性的画眉草细胞,这可能会提供一个治疗窗口针对这些分子的抗体消除瘤内Treg细胞但不是画眉草细胞。和他的同事描述了一个结合的抗体CD25但不阻止炎性- 2信号,提高了画眉草细胞功能的上下文中Treg细胞的损耗。最初的临床试验针对CD25有选择地实现Treg细胞消耗使用CD25的人源化单克隆抗体,daclizumab,先前批准的美国食品药品监督管理局,最初抑制免疫反应参与开发的在同种异体移植物排斥反应。

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