Concentration-dependent effects of immunomodulatory cocktails on the generation of leukemia-derived dendritic cells, DC mediated T-cell activation and on-target/off-tumor toxicity.

Journal: Frontiers in immunology
PMID:

Abstract

Acute myeloid leukemia (AML) remains a devastating diagnosis in clear need of therapeutic advances. Both targeted dendritic cells (DC) and particularly leukemia-derived dendritic cells (DC) can exert potent anti-leukemic activity. By converting AML blasts into immune activating and leukemia-antigen presenting cells, DC/DC-generating protocols can induce immune responses against AML blasts. Such protocols combine approved response modifiers (i.e., GM-CSF and PGE/OK-432/PGE) that synergistically improve the conversion of AML blasts into (mature) DC/DC. To guide potential clinical application of these response modifiers, we analyzed three different DC-generating protocols that combine a constant GM-CSF dose with varying concentrations of PGE (Kit-M), OK-432 (Kit-I), and PGE (Kit-K). Here, we specifically aimed to assess how different response modifier concentrations impact DC/DC generation, immune cell activation and leukemic blast lysis. We found that all immunomodulatory kits were effective in generating mature and leukemia-derived DCs from healthy and leukemic whole blood. For Kit-M, we noted optimal generation of DC-subsets at intermediary concentration ranges of PGE (0.25-4.0 µg/mL), which facilitated upregulation of activated and memory T-cells upon mixed lymphocyte culture, and efficient anti-leukemic activity in cytotoxicity assays. For Kit-I, we observed DC/DC generation and enhanced T- and immune cell activation across a broader range of OK-432 concentrations (5-40 µg/mL), which also facilitated improved leukemic blast killing. In conclusion, our results highlight that Kit-mediated DC/DC generation, immune cell activation and blast lysis are dependent on the concentration of response modifiers, which will guide future clinical development. Overall, DC-based immunotherapy represents a promising treatment strategy for AML patients.

Authors

  • Hazal Aslan Rejeski
    Department of Medicine III, LMU University Hospital, LMU Munich, Munich, Germany.
  • Anne Hartz
    Department of Medicine III, LMU University Hospital, LMU Munich, Munich, Germany.
  • Elias Rackl
    Department of Medicine III, LMU University Hospital, LMU Munich, Munich, Germany.
  • Lin Li
    Department of Medicine III, LMU University Hospital, LMU Munich, Munich, Germany.
  • Christoph Schwepcke
    Department of Medicine III, LMU University Hospital, LMU Munich, Munich, Germany.
  • Kai Rejeski
    Department of Medicine III, LMU University Hospital, LMU Munich, Munich, Germany.
  • Christoph Schmid
    Department of Hematology and Oncology, University Hospital of Augsburg, Augsburg, Germany.
  • Andreas Rank
    Bavarian Cancer Research Center (BZKF), Munich Site, Munich, Germany.
  • Jörg Schmohl
    Department of Hematology and Oncology, Diakonieklinikum Stuttgart, Stuttgart, Germany.
  • Doris Kraemer
    Department of Hematology and Oncology, St.-Josefs-Hospital, Hagen, Germany.
  • Peter Bojko
    Department of Hematology and Oncology, Rotkreuzklinikum Munich, Munich, Germany.
  • Helga Maria Schmetzer
    Department of Medicine III, LMU University Hospital, LMU Munich, Munich, Germany.