1222-Cellular Origins of Checkpoint Inhibitor

This research identifies the distinct cellular mechanisms behind checkpoint inhibitor pneumonitis (CIP) and radiation pneumonitis (RP) through advanced single-cell profiling of lung and blood samples. The study demonstrates that CIP is primarily driven by tissue-resident ZNF683hi CD8+ exhausted T cells, whereas RP originates from peripherally derived GZMKhi CD8+ T cells. These divergent biological pathways offer clear mechanistic differences that help clinicians distinguish between the two types of lung inflammation. By identifying specific cytological biomarkers, such as the CD8+ T/CD4+ T ratio, the findings provide a framework for more accurate differential diagnosis. Ultimately, these insights offer critical guidance for clinical decisions, specifically regarding the safety of immunotherapy rechallenge in lung cancer patients. The work establishes a robust molecular foundation for personalized management of treatment-related respiratory complications.References:Zhou X, Jiang Z, Ren Y, et al. Single-cell profiling unveils an exhaustion trajectory of ZNF683hi tissue-resident alveolar CD8+ T cells in checkpoint inhibitor pneumonitis[J]. Med, 2026.前往小宇宙评论区与主播互动