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Related Experiment Video

Updated: Jan 23, 2026

Generation of Myospheres From hESCs by Epigenetic Reprogramming
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Chronic stimulation drives human NK cell dysfunction and epigenetic reprograming.

Aimee Merino1, Bin Zhang1, Philip Dougherty1

  • 1Department of Medicine, University of Minnesota, Minneapolis, Minnesota, USA.

The Journal of Clinical Investigation
|June 19, 2019
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Summary

Chronic stimulation of adaptive Natural Killer (NK) cells, like memory T cells, leads to epigenetic reprogramming and dysfunction. This exhaustion in NK cells has implications for cancer immunotherapy strategies.

Keywords:
ImmunologyNK cells

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Area of Science:

  • Immunology
  • Cellular Biology
  • Epigenetics

Background:

  • Natural Killer (NK) cells expressing NKG2C and CD57 expand during human cytomegalovirus (HCMV) infection.
  • These adaptive NK cells share similarities with CD8+ memory T cells, including persistence and effector function.

Purpose of the Study:

  • To investigate if chronic stimulation induces epigenetic reprogramming and dysfunction in adaptive NK cells, similar to T cells.
  • To explore the potential for NK cell exhaustion in the context of chronic antigen exposure.

Main Methods:

  • Adaptive NK cells (CD3-CD56dimCD57+NKG2C+) were chronically stimulated using NKG2C agonistic antibodies and IL-15.
  • NK cell expression of checkpoint inhibitory receptors (LAG-3, PD-1) was analyzed.
  • Epigenetic modifications, including DNA methylation, were assessed genome-wide.

Main Results:

  • Chronic stimulation led to robust proliferation and activation of adaptive NK cells.
  • High expression of checkpoint inhibitory receptors LAG-3 and PD-1 was induced on chronically stimulated NK cells.
  • These NK cells exhibited dysfunction against tumor targets and showed genome-wide epigenetic reprogramming.

Conclusions:

  • Chronic stimulation of adaptive NK cells results in epigenetic reprogramming and functional exhaustion.
  • Exhausted NK cells present a potential target for cancer immunotherapy through checkpoint receptor blockade.