Fig. 3: MiR-142 deficit impairs T cell in vitro antileukemic activity.

a PB, BM and spleen T cells from Mir142^+/+BCR-ABL and Mir142^−/−BCR-ABL mice (BCR-ABL were induced by tet-off for 3 weeks) were subjected to scRNA-seq. Fifteen clusters were identified and annotated into distinct T cell subsets based on expression levels of naïve, memory, effector, and regulatory T gene markers. b Schematic design of experiment and results. LSKs from Mir142^−/−BCR-ABL mice were co-cultured with Mir142^+/+ T (WT-T) or Mir142^−/− T (homozygous KO; n = 4 samples per group; middle panel), or with WT-T or Mir142^+/− T (heterozygous KO; n = 6 samples per group; right panel) cells for 3 days, then viability of T and LSK cells was determined. c Cytokine levels of IFN-γ (n = 5 samples per group) and IL-2 (n = 4 per group), apoptosis (n = 4 per group), cell cycling (n = 3 per group), and cell growth (n = 4 per group) of human T cells from healthy donors with or without miR-142 KD were shown. d Levels of IFN-γ (n = 5 samples for CP CML and n = 6 for BC CML) and IL-2 (n = 6 samples per group) production in T cell subpopulations from CP CML or BC CML patients were shown. e Representative plots (left) and combined results (right) of CD4⁺ (n = 7 samples per group) and CD8⁺ (n = 8 for CP CML; n = 7 for BC CML) subpopulations in T cells from patients with BC CML or CP CML. f Spontaneous apoptosis of T cells from CP CML or BC CML patients (n = 5 samples per group). B/A BCR-ABL, PB peripheral blood, BM bone marrow, tet tetracycline, scRNA-seq single cell RNA sequencing, CM central memory, EM effector memory, Treg regulatory T, KD knock down, CML chronic myeloid leukemia, CP chronic phase, BC blast crisis. For b–f, comparison between two groups was performed by two-tailed, unpaired t-test. For b, comparisons among multi-groups were performed by one-way ANOVA and P values were corrected for multiple comparisons using Holm–Šídák method. Results shown represent mean ± SEM. Source data are provided as a Source Data file.