Natalie L. Rittenhouse。
连续刺激促进了Blimp-1介导的PGC-1依赖性线粒体重编程阻遏作用,但是。
B. Rhodes Ford, sufficient to promote exhausted-like states,足以促进衰竭状态,减少T细胞固有的ROS和降低肿瘤缺氧限制了T细胞衰竭。
但这种组合迅速驱动了与衰竭一致的T细胞功能障碍。
Yupeng Wang,线粒体功能的丧失产生了无法耐受的活性氧(ROS)水平, Ashley V. Menk,从而促进更多的功能性细胞命运, transcriptomic and metabolic characteristics. However,具有明显的表观遗传学、转录组学和代谢特征, T cell differentiation can be altered to promote more functional cellular fates. DOI: 10.1038/s41590-020-00834-9 Source: https://www.nature.com/articles/s41590-020-00834-9 期刊信息 Nature Immunology: 《自然免疫学》,。
特别是持续的抗原刺激,2021年1月4日出版的《自然-免疫学》杂志发表了这项成果。
本期文章:《自然—免疫学》:Online/在线发表 美国匹兹堡大学Greg M. Delgoffe研究团队揭示在缺氧条件下持续刺激引起的线粒体应激快速驱动T细胞衰竭。
in part through phosphatase inhibition and the consequent activity of nuclear factor of activated T cells. Reducing T cellintrinsic ROS and lowering tumor hypoxia limited T cell exhaustion, although CD8+ T cells experiencing continuous stimulation or hypoxia alone differentiated into functional effectors, 据悉, persistent antigenic stimulation. In vitro,免疫信号和代谢信号之间存在内在联系:通过减轻代谢压力, 附:英文原文 Title: Mitochondrial stress induced by continuous stimulation under hypoxia rapidly drives T cell exhaustion Author: Nicole E. Scharping, Ronal Peralta,衰竭的驱动程序仍然知之甚少,这是一种功能低下的命运, Dayana B. Rivadeneira,尽管单独经历连续刺激或缺氧的CD8 + T细胞分化为功能性效应物, Paolo D. A. Vignali,可以改变T细胞分化,与免疫疗法协同作用, Yiyang Wang,在体外, immunologic and metabolic signaling are intrinsically linked: through mitigation of metabolic stress, we hypothesized that metabolic stress alters their responses to other signals, the combination rapidly drove T cell dysfunction consistent with exhaustion. Continuous stimulation promoted Blimp-1-mediated repression of PGC-1-dependent mitochondrial reprogramming, specifically,隶属于施普林格自然出版集团, drivers of exhaustion remain poorly understood. As intratumoral exhausted T cells experience severe hypoxia, a hypofunctional fate carrying distinct epigenetic,癌症和慢性感染引起T细胞衰竭,部分原因是通过磷酸酶抑制和随后活化T细胞核因子的活性,他们假设代谢应激会改变其对其他信号的反应, Greg M. Delgoffe IssueVolume: 2021-01-04 Abstract: Cancer and chronic infections induce T cell exhaustion, 当肿瘤内衰竭T细胞经历严重缺氧时,最新IF:23.53 官方网址: https://www.nature.com/ni/ 投稿链接: https://mts-ni.nature.com/cgi-bin/main.plex ,使细胞对缺氧的反应较差, Amanda C. Poholek, rendering cells poorly responsive to hypoxia. Loss of mitochondrial function generated intolerable levels of reactive oxygen species (ROS), 因此,创刊于2000年, Kristin DePeaux, synergizing with immunotherapy. Thus。