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Targeting KIR Blockade in Multiple Myeloma: Trouble in Checkpoint Paradise?

Martin Felices1, Jeffrey S Miller1

  • 1Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota Masonic Cancer Center, Minneapolis, Minnesota. mille011@umn.edu mfelices@umn.edu.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|July 20, 2016
PubMed

Insights

Treatment with IPH2101 in smoldering multiple myeloma unexpectedly reduced natural killer (NK) cell function. This occurred via monocyte trogocytosis, despite the drug

Area of Science:

  • Immunology
  • Oncology
  • Hematology

Background:

  • Smoldering multiple myeloma is a precursor to active multiple myeloma.
  • Natural killer (NK) cells play a role in immune surveillance against cancer.
  • Inhibitory Killer cell immunoglobulin-like Receptors (KIRs) can suppress NK cell activity.

Purpose of the Study:

  • To investigate the effect of IPH2101, a KIR blockade therapy, on NK cell function in smoldering multiple myeloma.
  • To determine the mechanism underlying any observed changes in NK cell function.

Main Methods:

  • Monotherapy treatment with IPH2101 in patients with smoldering multiple myeloma.
  • Assessment of NK cell function.
  • Analysis of monocyte trogocytosis.

Main Results:

  • IPH2101 monotherapy resulted in a reduction of NK cell function.
  • This reduction was mediated by monocyte trogocytosis.
  • The intended enhancement of NK cell function was not observed.

Conclusions:

  • KIR blockade with IPH2101 can paradoxically impair NK cell function in smoldering multiple myeloma.
  • Monocyte trogocytosis is a key mechanism involved in this NK cell dysfunction.
  • These findings have implications for the development of immunotherapies targeting NK cells.

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