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Nature: 免疫细胞中发现重要肿瘤抑制因子

2017-12-07  来源:艾兰博曼医学网  作者:鱼会飞  编辑:陌莉花开
导读
最近,科学家在免疫系统的T细胞中发现了一个“紧急切断开关”。这项新的研究可能会为那些免疫细胞缺陷触发的T细胞霍奇金淋巴瘤患者带来新的治疗方法。


最近,科学家在免疫系统的T细胞中发现了一个“紧急切断开关”。这项新的研究可能会为那些免疫细胞缺陷触发的T细胞霍奇金淋巴瘤患者带来新的治疗方法。

T细胞在体内通常角色是负责检测和杀死癌细胞。T细胞时人体防御癌症的重要组成部分。然而,当T细胞本身在其基因组中出现缺陷时,这种角色扮演可能会出现问题。如果基因缺陷出现在负责细胞生长的基因组区域,则T细胞本身可能变成无限增殖的肿瘤细胞。

当T细胞的金银组中出现缺陷时,正是导致T细胞非霍奇金淋巴瘤发生的原因。这种侵袭性的淋巴瘤治疗率很低。JürgenRuland教授正在与他的团队一起研究这些癌症的分子机制,以便更有效地治疗这些癌症,并将最新的研究结果发表在《Nature》上。

科学家研究发现,有基因缺陷的T细胞又一个成为肿瘤抑制因子的紧急切断开关。研究证实,PD-1蛋白可以在早期关闭有缺陷的T细胞,从而租店他们成为肿瘤细胞。研究人员首先在T细胞非霍奇金淋巴瘤的小鼠模型中发现了PD-1的这种功能,并且还对这一机制进行了解释:PD-1被T细胞生长缺陷基因激活,然后对其进行抑制。因此,PD-1起着关闭开关的作用,以防止有缺陷的T细胞不受生长控制。

科学家还成功揭示了T细胞非霍奇金淋巴瘤侵袭性强的原因。他们对150名患者的基因数据进行了分析:“根据先前的研究结果,我们有意识的对PD-1进行了关注”。其中超过30%的患者其和PD-1相互作用的区域发生了变化。这将给肿瘤患者带来灾难性的后果,将会带来灾难性的后果。因为它们不能起到“紧急切断”的作用。所以患者的T细胞无限增殖。这些患者可以通过逆转PD-1的信号丢失的药物来破坏肿瘤细胞,这种药物目前已在其他形式的抗肿瘤治疗中实现。所以,这对于非霍奇金淋巴瘤的治疗来说也是一种可以考虑的治疗方法。

英文原文:

A team from Technical University of Munich has discovered an "emergency shut-off switch" in immune system T cells. Their results could lead to new therapies against T cell non-Hodgkin's lymphoma triggered by defective immune cells.

In the body, T cells are usually responsible for detecting and killing cancer cells. However, problems can arise when a T cell itself develops a defect in its genome. If the defect affects areas of the genome responsible for cell growth, referred to as oncogenes, the T cell itself can become an uncontrollably dividing tumor cell. In addition, the T cell, an important part of the body's defense against cancer, fails.

This is exactly what occurs in T cell non-Hodgkin's lymphoma. This aggressive form of lymphoma has a very low rate of successful treatment and afflicts approximately one out of every 100,000 persons in Germany. Prof. Jürgen Ruland, Director of the TUM Institute for Clinical Chemistry and Pathobiochemistry is working together with his team to understand the molecular mechanisms of these cancers in order to treat them more effectively.

In their new study, currently published in the journal Nature, the scientists were able to show that the defective T cells have an emergency shut-off switch, referred to as a tumor suppressor. They ascertained that the protein PD-1 can turn off defective T cells at an early stage and thus prevent them from becoming tumor cells. The researchers first discovered this function of PD-1 in a mouse model for T cell non-Hodgkin's lymphoma and were also able to explain the mechanism: PD-1 is activated by defects in genes for cell growth, known as oncogenes, and then suppresses the effect of these genes using additional proteins. Thus, it functions as a shut-off switch to prevent the uncontrolled growth of defective T cells.

The scientists also successfully resolved the question of why many T cell non-Hodgkin's lymphomas are so aggressive, in spite of this protective function. They investigated genetic data sets from 150 patients: "Based on our previous results, we intentionally focused closely on PD-1. In individual groups more than 30 percent of the patients exhibited changes in the regions of the genome that interfered with the production of PD-1. This has disastrous consequences in the tumor—PD-1 no longer functions as an 'emergency shut-off' for them. The diseased T cells can reproduce uncontrollably," says Tim Wartewig, lead author of the study.

"These patients could be helped by medications that reverse the loss of PD-1 signaling and thereby destroy the tumor cells. This type of medication already exists for other forms of cancer. In our opinion, use with T cell non-Hodgkin's lymphoma should also be considered," says Jürgen Ruland. The scientists therefore recommend investigating individual differences in tumors before making decisions about which medication is to be administered.



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