Exhausted T(Tex)cells are a distinct subset of T cells that arise in response to prolonged antigen exposure during chronic infections or cancer.Although Tex cells exhibit reduced functionality,they still retain some p...Exhausted T(Tex)cells are a distinct subset of T cells that arise in response to prolonged antigen exposure during chronic infections or cancer.Although Tex cells exhibit reduced functionality,they still retain some protective abilities.Exhausted CD8+T cells are a heterogeneous group consisting of four subsets:progenitor,intermediate,effector,and terminally exhausted.Each subset is characterized by distinct transcriptional,epigenetic,and functional traits[1].Recent studies have indicated that the progenitor and intermediate Tex subsets are mainly responsible for the proliferative surge observed during anti-PD-1 immunotherapy,which results in the production of a large pool of functional effector cells,thereby sustaining the antitumor immune response[2].However,blocking the PD-1 pathway alone typically fails to achieve lasting disease control in most patients.Simultaneous blockade of PD-1 and other immune checkpoint receptors can enhance CD8+T-cell-mediated immunity,leading to more effective treatment outcomes.展开更多
基金supported by an intramural grant from KIST to YP,as well as grants from the National Research Foundation of Korea(NRF)funded by the Korean government(MSIT)(NRF-2020M3A9G7103935 and RS-2024-00338729 to HJ and RS-2024-00337093 to YP).
文摘Exhausted T(Tex)cells are a distinct subset of T cells that arise in response to prolonged antigen exposure during chronic infections or cancer.Although Tex cells exhibit reduced functionality,they still retain some protective abilities.Exhausted CD8+T cells are a heterogeneous group consisting of four subsets:progenitor,intermediate,effector,and terminally exhausted.Each subset is characterized by distinct transcriptional,epigenetic,and functional traits[1].Recent studies have indicated that the progenitor and intermediate Tex subsets are mainly responsible for the proliferative surge observed during anti-PD-1 immunotherapy,which results in the production of a large pool of functional effector cells,thereby sustaining the antitumor immune response[2].However,blocking the PD-1 pathway alone typically fails to achieve lasting disease control in most patients.Simultaneous blockade of PD-1 and other immune checkpoint receptors can enhance CD8+T-cell-mediated immunity,leading to more effective treatment outcomes.
