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Oxidized LDL Induces Pro-Inflammatory Transcriptomic and Epigenomic Responses in Human CD4+ T Cells.

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FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
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Oxidized low-density lipoprotein (ox-LDL) alters CD4+ T cells, promoting inflammation and contributing to coronary artery disease (CAD) pathogenesis. This study reveals ox-LDL

Keywords:
LDL lipoproteinsatherosclerosisepigenomicshelper‐inducer T‐lymphocytesinflammationtranscriptome

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Area of Science:

  • Immunology
  • Cardiovascular Research
  • Genomics

Background:

  • Elevated low-density lipoprotein cholesterol (LDL-C) is a major risk factor for coronary artery disease (CAD).
  • CD4+ T cells infiltrate atherosclerotic lesions, but their response to oxidized LDL (ox-LDL) is not well understood.
  • CAD pathogenesis involves complex interactions between genetic and lifestyle factors.

Purpose of the Study:

  • To investigate the transcriptomic and epigenomic effects of ox-LDL on activated human CD4+ T cells.
  • To identify molecular mechanisms linking ox-LDL exposure to CAD development.
  • To explore the disease relevance of ox-LDL-induced changes in CD4+ T cells.

Main Methods:

  • Multiomic analysis (transcriptomics and epigenomics) of human CD4+ T cells stimulated with ox-LDL.
  • Chromatin accessibility assays (ATAC-seq) to map regulatory regions.
  • Integration of multiomic data with CAD-associated genetic variants.
  • Identification of key transcription factors involved in ox-LDL response.

Main Results:

  • Ox-LDL induces a pro-inflammatory CD4+ T cell phenotype with increased cytokine production.
  • Ox-LDL causes widespread changes in chromatin accessibility, particularly at promoter regions.
  • NRF1 and SP1 transcription factors mediate ox-LDL-induced gene expression changes, while AP-1 activity decreases.
  • CAD-associated single nucleotide polymorphisms are enriched in ox-LDL-regulated accessible chromatin regions.

Conclusions:

  • Oxidized LDL plays a disease-relevant role in the atherogenic conditioning of CD4+ T cells.
  • Understanding ox-LDL's impact on CD4+ T cells offers insights into CAD pathogenesis.
  • Targeted therapies for CAD may be developed by considering these cell-type-specific interactions.