摘要
The thymus provides specialized signals that support and guide the development of precursor cells into various T-cell lineages,including conventionalαβT cells comprising the CD4^(+) and CD8^(+) T-cell subsets that are key mediators of adaptive immunity.Within the thymus,a complex network of persistent T-cell receptor(TCR)activation,cytokine signals,and transcription factors dictates the development of CD4^(+) and CD8^(+) T cells.1 The fate commitment of CD4^(+) and CD8^(+) T-cell lineages is reciprocally orchestrated by the ThPOK-and Runx3-dependent transcriptome.2,3 In the periphery,mature CD4^(+) or CD8^(+) T cells are activated by specific antigens bound to major histocompatibility complex class II(MHC-II)or I(MHC-I),respectively,which facilitates their clonal expansion and effector function in defense against pathogen infection.While the dichotomy of CD4 and CD8 lineage decisions is considered to be stable in mature T cells,whether and how pathogens reprogram lineage commitment during an immune response remain unclear.In this issue of Cellular and Molecular Immunology,4 Robins et al.demonstrated that Vps34/Atg7-dependent autophagy inhibits the generation of MHC-II-restricted CD4−CD8^(+) T cells by restraining Runx3 expression in effector CD4^(+) T cells upon pathogen infection(Fig.1).
