B7-H3 suppresses CD8<sup>+</sup> T cell immunologic function through reprogramming glycolytic metabolism
Yulu Wu, Wenzhe Han, Xiufa Tang, Jiyuan Liu, Zhiyong Guo, Zhangao Li, Chenchen Cai, Lin Que
Abstract
T cell functions within the tumor microenvironment and its impact on tumorigenicity. We also demonstrate that glycolysis inhibition can be mitigated by exogenous glucose supplementation. Mechanistically, our study suggests B7-H3's influence on metabolism might be mediated through the phosphoinositide3-kinase (PI3K)/ protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) signaling pathway. This research unveils how B7-H3 affects immune functions via metabolic reprogramming.
Topics & Concepts
PI3K/AKT/mTOR pathwayCancer researchBiologyImmune systemTumor microenvironmentCD8GlycolysisT cellAnaerobic glycolysisCell biologySignal transductionMetabolismImmunologyEndocrinologyCancer Immunotherapy and BiomarkersCAR-T cell therapy researchImmune cells in cancer