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PD-1(programmed death-1)通过负调控T细胞功能和存活维持免疫稳态。阻断PD-1信号会放大移植物抗宿主反应(GVHD),而目前对于PD-1的抑制功能与T细胞代谢的相互作用尚不明确。本文作者发现,在同种异体骨髓移植之后,小鼠和人的同种异体反应T细胞均伴随着PD-1及ROS的上调。这种PD-1和ROS高表达的特征仅存在于同种异体反应T细胞,而不存在于同基因的T细胞中。阻断PD-1信号通路会减少线粒体ROS和总细胞ROS,PD-1介导的ROS增加源自脂肪酸氧
PD-1 (programmed death-1) maintains immune homeostasis by negatively regulating T cell function and survival. Blocking PD-1 signaling amplifies graft-versus-host response (GVHD), but the interaction between PD-1 inhibition and T-cell metabolism is unclear. The authors found that allogeneic T cells from mice and humans were accompanied by upregulation of PD-1 and ROS after allogeneic bone marrow transplantation. This feature of high expression of PD-1 and ROS is present only in alloreactive T cells but not in syngeneic T cells. Blocking the PD-1 signaling pathway reduced mitochondrial ROS and total cellular ROS, and PD-1 -mediated increases in ROS were derived from fatty acid oxygen