Causal roles of immune cells in cardiovascular diseases: A Mendelian randomization (MR) study

Virak Vicheth1, Chongbin Zhong1, Junjie Guan1

  • 1Department of Cardiology, Laboratory of Heart Center, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.

PubMed

Insights

This study reveals key immune cell connections to cardiovascular disease (CVD) risk. Certain T-cell and B-cell phenotypes may protect against CVD, while others increase risk, offering new insights into disease mechanisms.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Genetics

Background:

  • Cardiovascular diseases (CVDs) are a leading cause of mortality globally, yet their underlying mechanisms remain incompletely understood.
  • Investigating the role of circulating activated immune cells may elucidate pathological pathways in CVD development.

Purpose of the Study:

  • To explore the potential causal links between various immune cell phenotypes and the risk of developing cardiovascular diseases.
  • To identify specific immune signatures associated with either protection or increased risk of CVD.

Main Methods:

  • A two-sample Mendelian randomization analysis was conducted using publicly available genetic data.
  • Examined 731 immune phenotypes, including relative cell counts, absolute cell counts, morphological parameters, and median fluorescence intensities.
  • Sensitivity analyses were performed to ensure the robustness and reliability of the findings.

Main Results:

  • Identified significant associations between specific immunophenotypes and CVD risk.
  • Activated and secretory CD4+ regulatory T-cells (Tregs) showed a protective effect (OR: 0.757).
  • Increased CVD risk was associated with CD80 on myeloid dendritic cells (OR: 1.181) and specific proportions of CD8+ T-cells.

Conclusions:

  • Specific immune cell phenotypes are significantly correlated with cardiovascular disease risk.
  • Findings provide novel perspectives for future clinical research into CVD pathogenesis and potential therapeutic targets.
Abstract