Mass-cytometry files (.fcs) from Aziez et al,. Pro-inflammatory role of granzyme K producing bystander CD8 T cells in acute myeloid leukemia

Mass Cytometry (CyTOF) Data from Aziez et al., "Pro-inflammatory Role of Granzyme K-Producing Bystander CD8 T Cells in Acute Myeloid Leukemia" The provided files (.fcs) contain mass cytometry (CyTOF) data pre-gated on live CD8+ T cells isolated from peripheral blood mononuclear cells (PBMCs) or bone marrow (BM) of newly diagnosed Acute Myeloid Leukemia (AML) patients. AbstractAcute Myeloid Leukemia (AML) is a heterogeneous group of blood malignancies with a five-year survival rate below 30%, underscoring the urgent need for more effective therapeutic strategies. While T cell-based immunotherapies have shown remarkable success in solid tumors, the role of CD8+ T cells in AML remains poorly understood.In this study, we analyzed the composition, antigenic specificity, and function of CD8+ T cells in paired blood and bone marrow samples from AML patients. Unlike in solid tumors, we did not identify exhausted CD8+ T cells. Instead, we observed a distinct population of functional CD69+ CD8+ T cells specifically enriched in the bone marrow. These cells primarily recognized non-tumor antigens, including epitopes derived from Epstein–Barr virus (EBV) and cytomegalovirus (CMV). Notably, this bystander CD8+ T cell population exhibited high expression of Granzyme K, a molecule found at elevated levels in the bone marrow of AML patients. Rather than inducing leukemic cell death, Granzyme K promoted the secretion of IL-8, a pro-inflammatory cytokine known to contribute to AML pathology.These findings suggest that, instead of mounting an anti-tumor immune response, these CD8+ T cells may foster a pro-inflammatory microenvironment that exacerbates AML progression and severity. This highlights a potential therapeutic avenue focused on inhibiting pro-inflammatory CD8+ T cell activity and targeting Granzyme K in combination with existing treatments.