Oleate-Mediated Enhancement of Human Natural Killer Cell Function (UCLA Case No. 2024-180)

UCLA researchers in the Department of Microbiology, Immunology and Molecular Genetics have discovered a novel approach to boost natural killer cell function through fatty acid supplementation.

BACKGROUND: Natural killer (NK) cells are part of the body’s defense system that hunts down and kills cells that are infected by viruses or have become cancerous. People lacking functional NK cells are more vulnerable to viruses, sometimes leading to early death from widespread infection. In humans, different types of NK cells have varying abilities to produce IFN-gamma and kill infected cells. Understanding how NK cells develop and function is critical, as mutations in certain genes can lead to deficiencies in these cells and increase susceptibility to infections.

INNOVATION: Researchers lead by Dr. Timothy O’Sullivan made a novel discovery which can enhance NK cell function by targeting the MEF2C gene. This gene plays a critical role in NK cell development, cytokine production, and killing infected cells. Researchers showed that defects in MEF2C can impair NK cell function, but supplementation with fatty acids can help restore their ability to fight off infections. Fatty acid supplementation is a promising and safe method to treat NK cell function deficiency in various immunodeficiency disorders.

POTENTIAL APPLICATIONS:

  • Development of novel therapies for boosting NK cell activity.
  • Development of a method to improve immune responses against viruses.

ADVANTAGES:

  • Understanding of the molecular pathways underlying MEF2C-mediated regulation of NK cells has clinical implications for the diagnosis and treatment of immune disorders.
  • Identification of MEF2C as a critical regulator of NK cell function.

DEVELOPMENT-TO-DATE: This research was conducted in MEF2C haploinsufficient patients and mice.

Related Papers (from the inventors only): Li, J.H., Zhou, A., Lee, C.D. et al. MEF2C regulates NK cell effector functions through control of lipid metabolism. Nat Immunol 25, 778–789 (2024). https://doi.org/10.1038/s41590-024-01811-2

Patent Information: