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Related Concept Videos

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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...
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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
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Related Experiment Video

Updated: Jun 24, 2025

Flow Cytometry-based Assay for the Monitoring of NK Cell Functions
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DOT1L maintains NK cell phenotype and function for optimal tumor control.

Harrison Sudholz1, Iona S Schuster2, Momeneh Foroutan3

  • 1Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry, Monash University, Clayton, VIC 3800, Australia.

Cell Reports
|June 12, 2024
PubMed
Summary

The histone methyltransferase DOT1L prevents natural killer (NK) cells from converting into a subset linked to poor tumor control. Loss of DOT1L impairs NK cell function and solid tumor control.

Keywords:
CP: CancerCP: Immunology

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Area of Science:

  • Immunology
  • Cancer Biology
  • Epigenetics

Background:

  • Histone methyltransferases (HMTs) regulate gene expression, but their role in natural killer (NK) cell biology within the tumor microenvironment (TME) is unclear.
  • NK cells are critical for anti-tumor immunity, and their function can be modulated by the TME.

Purpose of the Study:

  • To investigate the role of the HMT DOT1L in NK cell biology within the TME.
  • To determine if DOT1L influences NK cell conversion to other immune cell subsets.

Main Methods:

  • Genetic deletion of Dot1l in NKp46-expressing cells.
  • Analysis of NK cell phenotype and transcriptional profiles.
  • Assessment of NK cell function in the context of solid tumors.

Main Results:

  • DOT1L limits the conversion of NK cells to CD49a+ CD49b+ intILC1s, a subset associated with impaired tumor control.
  • Loss of DOT1L causes NK cells to skew towards an intILC1 phenotype, even without TGF-β stimulation.
  • DOT1L-deficient NK cells exhibit transcriptional profiles similar to intILC1s and ILC1s, leading to altered responses and reduced solid tumor control.

Conclusions:

  • DOT1L is essential for maintaining NK cell identity and function within the TME.
  • Targeting DOT1L could offer a strategy to prevent detrimental NK cell conversion in cancer immunotherapy.