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Updated: Feb 2, 2026

A Novel Feeder-free System for Mass Production of Murine Natural Killer Cells In Vitro
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Published on: January 9, 2018

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Natural killer cell-based immunotherapy: a new fighter against melanoma?

Vincas Urbonas1, Giedre Smailyte2, Greta V Urbonaite3

  • 1Laboratory of Clinical Oncology, Department of Medical Oncology.

Melanoma Research
|November 20, 2018
PubMed

Insights

A new monoclonal antibody targeting MICA and MICB shedding blocks cancer immune evasion. This approach reactivates Natural Killer (NK) cells, restoring anticancer immunity and reducing melanoma progression in mice.

Area of Science:

  • Immunology
  • Oncology
  • Cancer Biology

Background:

  • Cancer cells exhibit altered surface protein expression, a hallmark of malignant transformation.
  • Natural Killer (NK) cells identify and eliminate stressed cells, including cancer cells, via activating and inhibitory receptors.
  • Major histocompatibility complex class I polypeptide-related sequence A and B (MICA and MICB) are ligands recognized by the NK cell receptor NKG2D, but cancer cells often shed these proteins to evade NK cell detection.

Purpose of the Study:

  • To investigate the therapeutic potential of targeting the proteolytic shedding of MICA and MICB.
  • To evaluate the efficacy of a monoclonal antibody designed to inhibit MICA/MICB shedding in reducing melanoma progression.
  • To assess the impact of this antibody on NK cell activation and anticancer immunity.

Main Methods:

  • Development of a monoclonal antibody targeting the shedding site of MICA and MICB proteins.
  • Administration of the antibody in immunocompromised and immune-competent mouse models of melanoma.
  • Assessment of tumor progression, MICA/MICB levels, and NK cell activity (NKG2D activation).

Main Results:

  • The monoclonal antibody targeting MICA/MICB shedding significantly reduced melanoma progression in both immunocompromised and immune-competent mouse models.
  • This therapeutic strategy prevented the proteolytic shedding of MICA and MICB, maintaining essential immunostimulatory ligands.
  • The approach successfully restored NK cell-driven anticancer immunity by reactivating NKG2D.

Conclusions:

  • Targeting the proteolytic shedding of MICA and MICB with a specific monoclonal antibody is a promising strategy to overcome cancer immune evasion.
  • This method restores NK cell recognition and cytotoxic function against tumors by maintaining NKG2D ligand expression.
  • The findings suggest a novel therapeutic avenue for enhancing NK cell-based immunotherapy in melanoma and potentially other cancers.

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