Role of unusual CD4+ CD28- T cells in acute coronary syndrome

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Updated: May 31, 2026

Isolation and Identification of Extravascular Immune Cells of the Heart
08:24

Isolation and Identification of Extravascular Immune Cells of the Heart

Published on: August 23, 2018

Wenjie Sun1, Lihui Zheng, Lijuan Huang

  • 1Department of Laboratory Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, People's Republic of China.

Molecular Biology Reports
|June 23, 2011
PubMed

Insights

CD4(+) CD28(-) T cells are implicated in acute coronary syndrome (ACS) plaque ruptures. Targeting these cells may offer new therapies for preventing life-threatening cardiovascular events.

Area of Science:

  • Cardiology
  • Immunology
  • Molecular Biology

Background:

  • Acute coronary syndrome (ACS) arises from occlusive thrombus due to atherosclerotic plaque rupture or erosion.
  • CD4(+) CD28(-) T cells are present in atherosclerotic plaques and circulation of ACS patients.
  • These cells are increasingly recognized for their role in plaque instability.

Purpose of the Study:

  • To review the generation, phenotypic, and functional characteristics of CD4(+) CD28(-) T cells in ACS.
  • To explore the relevance of these cells in cardiovascular event development.
  • To highlight potential therapeutic strategies targeting CD4(+) CD28(-) T cells.

Main Methods:

  • Review of current literature on CD4(+) CD28(-) T cell generation and function.
  • Analysis of phenotypic and functional data related to cardiovascular events.
  • Discussion of therapeutic implications.

Main Results:

  • CD4(+) CD28(-) T cells are an unusual, expanded helper T cell subset in ACS.
  • These cells exhibit characteristics contributing to plaque rupture and cardiovascular events.
  • Their presence is linked to the pathogenesis of ACS.

Conclusions:

  • CD4(+) CD28(-) T cells play a significant role in ACS pathogenesis and plaque rupture.
  • Understanding their specific characteristics is crucial for cardiovascular event development.
  • Targeting the CD4(+) CD28(-) T cell subset presents a promising therapeutic avenue for ACS.

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