仿形(计算机编程)
转录组
细胞
肺结核
肺结核
细胞生物学
受体
计算生物学
生物
医学
遗传学
病理
基因
计算机科学
基因表达
操作系统
作者
Wen Zhu,Lin Wang,Hui Ma,Leilei Li,Laiyi Wan,Lei Shi,Hongwei Li,Hui Chen,Wenjun Hao,Shu Song,Qiang Xue,Yutong Wei,Feng Li,Jianqing Xu,Shulin Zhang,Ka-Wing Wong,Yanzheng Song
标识
DOI:10.1016/j.jinf.2024.106158
摘要
Tuberculosis-affected lungs with chronic inflammation harbor abundant immunosuppressive immune cells but the nature of such inflammation is unclear. Dysfunction in T cell exhaustion, while implicated in chronic inflammatory diseases, remains unexplored in tuberculosis. Given that immunotherapy targeting exhaustion checkpoints exacerbates tuberculosis, we speculate that T cell exhaustion is dysfunctional in tuberculosis. Using integrated single-cell RNA sequencing and T cell receptor profiling we reported defects in exhaustion responses within inflamed tuberculosis-affected lungs. Tuberculosis lungs demonstrated significantly reduced levels of exhausted CD8+ T cells and exhibited diminished expression of exhaustion-related transcripts among clonally expanded CD4+ and CD8+ T cells. Additionally, clonal expansion of CD4+ and CD8+ T cells bearing T cell receptors specific for CMV was observed. Expanded CD8+ T cells expressed the cytolytic marker GZMK. Hence, inflamed tuberculosis-affected lungs displayed dysfunction in T cell exhaustion. Our findings likely hold implications for understanding the reactivation of tuberculosis observed in patients undergoing immunotherapy targeting the exhaustion checkpoint.
科研通智能强力驱动
Strongly Powered by AbleSci AI