生物
细胞
细胞毒性T细胞
T细胞
细胞生物学
计算生物学
癌症研究
免疫学
遗传学
免疫系统
体外
作者
Katharine E. Block,Stephen C. Jameson
出处
期刊:Immunity
[Elsevier]
日期:2024-06-01
卷期号:57 (6): 1184-1186
标识
DOI:10.1016/j.immuni.2024.05.014
摘要
The mechanisms that make and break CD8+ T cell tolerance to self-antigens remain unclear. In this issue of Immunity, Van Der Byl et al. show that tolerant CD8+ T cells rapidly adopt an epigenetically and transcriptionally distinct cell state and exhibit impaired protein translation. Breaking tolerance requires both inflammation and increased antigen exposure to augment MYC expression and restore translation. The mechanisms that make and break CD8+ T cell tolerance to self-antigens remain unclear. In this issue of Immunity, Van Der Byl et al. show that tolerant CD8+ T cells rapidly adopt an epigenetically and transcriptionally distinct cell state and exhibit impaired protein translation. Breaking tolerance requires both inflammation and increased antigen exposure to augment MYC expression and restore translation. The CD8+ T cell tolerance checkpoint triggers a distinct differentiation state defined by protein translation defectsVan Der Byl et al.ImmunityMay 21, 2024In BriefSteady-state antigen recognition triggers tolerant CD8+ T cell states that restrain autoimmunity and limit anti-cancer immunity. The relationship between tolerant states and other differentiation states remains unclear. Van Der Byl et al. demonstrate that tolerance triggers a transcriptionally and epigenetically distinct differentiation trajectory. The synergistic actions of strong TCR signaling and inflammation are required to override the tolerance checkpoint. Full-Text PDF
科研通智能强力驱动
Strongly Powered by AbleSci AI