CD80
CD86
TFEB
抗原
细胞毒性T细胞
细胞生物学
化学
内吞作用
免疫疗法
MHC I级
抗原提呈细胞
树突状细胞
肿瘤抗原
免疫系统
抗原呈递
交叉展示
CD8型
癌症免疫疗法
T细胞
免疫学
CD40
生物
转录因子
细胞
生物化学
体外
基因
作者
Jingwei Ma,Keke Wei,Huafeng Zhang,Ke Tang,Fei Li,Tianzhen Zhang,Junwei Liu,Pingwei Xu,Yuandong Yu,Weiwei Sun,Liyan Zhu,Jie Chen,Li Zhou,Xiaoyu Liang,Jiadi Lv,Roland Fiskesund,Yuying Liu,Bo Huang
标识
DOI:10.1158/2326-6066.cir-17-0716
摘要
Abstract Tumor cell–derived microparticles (T-MP) contain tumor antigen profiles as well as innate signals, endowing them with vaccine potential; however, the precise mechanism by which DCs present T-MP antigens to T cells remains unclear. Here, we show that T-MPs activate a lysosomal pathway that is required for DCs presenting tumor antigens of T-MPs. DCs endocytose T-MPs to lysosomes, where T-MPs increase lysosomal pH from 5.0 to a peak of 8.5 via NOX2-catalyzed reactive oxygen species (ROS) production. This increased pH, coupled with T-MP–driven lysosomal centripetal migration, promotes the formation of MHC class I–tumor antigen peptide complexes. Concurrently, endocytosis of T-MPs results in the upregulation of CD80 and CD86. T-MP–increased ROS activate lysosomal Ca2+ channel Mcoln2, leading to Ca2+ release. Released Ca2+ activates transcription factor EB (TFEB), a lysosomal master regulator that directly binds to CD80 and CD86 promoters, promoting gene expression. These findings elucidate a pathway through which DCs efficiently present tumor antigen from T-MPs to CD8+ T cells, potentiating T-MPs as a novel tumor cell–free vaccine with clinical applications. Cancer Immunol Res; 6(9); 1057–68. ©2018 AACR.
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