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EPA Induces an Anti-Inflammatory Transcriptome in T Cells, Implicating a Triglyceride-Independent Pathway in

Nathalie A Reilly1, Koen F Dekkers2, Jeroen Molenaar2

  • 1Molecular Epidemiology, Department of Biomedical Data Sciences, Leiden University Medical Center, Leiden, the Netherlands; Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.

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|March 26, 2025
PubMed
Summary
This summary is machine-generated.

Eicosapentaenoic acid (EPA) reduces cardiovascular risk by altering CD4+ T cell gene expression. EPA specifically downregulates immune genes and upregulates oxidative stress defenses, revealing a novel anti-inflammatory mechanism.

Keywords:
T cellsatherosclerosiseicosapentaenoic acidoleic acidpalmitic acidtranscriptomics

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cardiovascular Science

Background:

  • Purified eicosapentaenoic acid (EPA) intake reduces cardiovascular disease risk in high triglyceride patients.
  • The precise mechanism underlying EPA's cardioprotective effects remains incompletely understood.

Purpose of the Study:

  • To investigate the molecular mechanisms by which EPA influences CD4+ T cell function.
  • To elucidate the transcriptomic and epigenetic changes induced by EPA in immune cells.

Main Methods:

  • Non-activated CD4+ T cells were exposed to EPA, oleic acid, palmitic acid, or control.
  • RNA sequencing and ATAC-sequencing were performed after 48 hours of exposure.
  • Transcription factor binding was analyzed using footprinting.

Main Results:

  • EPA exposure downregulated immune response genes (e.g., HLA-DRA, CD69, IL2RA) and upregulated oxidative stress prevention genes (e.g., NQO1).
  • Transcription factor analysis revealed decreased GATA3 and PU.1 binding, and increased REV-ERB binding.
  • Observed effects were specific to EPA, indicating a targeted molecular response.

Conclusions:

  • EPA induces an anti-inflammatory transcriptomic landscape in CD4+ T cells.
  • These EPA-mediated changes in T cells likely contribute to its beneficial effects on cardiovascular health.
  • EPA's impact on T cell gene expression offers a potential therapeutic target for cardiovascular disease prevention.