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Kmt2c and Kmt2d histone methyltransferase deficiencies compromise macrophage function
Burcu Al1, Yerin Jung1, Yubell P Alvarez1
1Immunology and Metabolism, Life and Medical Sciences Institute, University of Bonn, Bonn, Germany.
Journal of Leukocyte Biology
|August 11, 2026
Summary
Histone methylation by Kmt2c and Kmt2d is crucial for innate immunity. Their deficiency impairs macrophage function, cytokine response, and phagocytosis, altering energy metabolism.
Area of Science:
- Epigenetics
- Immunology
- Molecular Biology
Background:
- Histone (H) 3 lysine (K) 4 methylation is vital for innate immunity.
- The specific roles of H3K4 methyltransferases Kmt2c and Kmt2d in innate immunity require further elucidation.
Purpose of the Study:
- To investigate the impact of Kmt2c and Kmt2d deficiency on innate immune cell function.
- To understand the epigenetic regulation of macrophage biology by Kmt2c and Kmt2d.
Main Methods:
- Conditional knockout (KO) mouse models were utilized.
- Functional, transcriptomic, and metabolic analyses were performed on macrophages.
Main Results:
- Kmt2c or Kmt2d deficiency in macrophages resulted in impaired pro-inflammatory cytokine production.
- Phagocytotic capacity was reduced in Kmt2c/Kmt2d-deficient macrophages.
- Macrophage energy metabolism shifted towards glycolysis upon Kmt2c/Kmt2d loss.
Conclusions:
- Kmt2c and Kmt2d are critical epigenetic regulators of innate immune cell function.
- Disrupted H3K4 methylation impacts macrophage responses and metabolism, highlighting the link between epigenetics and immunity.
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