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Flow Cytometry Analysis of Immune Cells Within Murine Aortas
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PD-1 and Tim-3 Pathways Regulate CD8+ T Cells Function in Atherosclerosis.

Ming-Ke Qiu1, Song-Cun Wang2, Yu-Xin Dai1

  • 1Department of General Surgery, Xinhua Hospital, Shanghai JiaoTong University, School of Medicine, Shanghai, China.

Plos One
|June 3, 2015
PubMed
Summary
This summary is machine-generated.

Programmed cell death-1 (PD-1) and T cell immunoglobulin and mucin domain 3 (Tim-3) co-expression on CD8+ T cells is elevated in atherosclerosis (AS) patients. This suggests a regulatory role for these pathways in AS pathogenesis.

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Area of Science:

  • Immunology
  • Cardiovascular Research
  • Cell Biology

Background:

  • T cell-mediated immunity is crucial in atherosclerosis (AS) development.
  • The specific roles of CD8+ T cells in AS are not fully understood.
  • Programmed cell death-1 (PD-1) and T cell immunoglobulin and mucin domain 3 (Tim-3) are key regulators of T cell function.

Purpose of the Study:

  • To investigate the expression and function of PD-1 and Tim-3 on CD8+ T cells in human AS.
  • To elucidate the role of PD-1 and Tim-3 co-expression in CD8+ T cell subsets and cytokine production within AS.

Main Methods:

  • Flow cytometry to analyze PD-1 and Tim-3 expression on CD8+ T cells in AS patients.
  • Characterization of PD-1+ Tim-3+ CD8+ T cell subsets (TCM, CD127 expression).
  • Assessment of cytokine production (anti- and pro-atherogenic) and the impact of PD-1/Tim-3 blockade.

Main Results:

  • PD-1 and Tim-3 co-expression is significantly upregulated on CD8+ T cells in AS patients.
  • PD-1+ Tim-3+ CD8+ T cells are enriched in the central T cell memory (TCM) subset and exhibit high proliferative activity.
  • Co-expression correlates with altered anti- and pro-atherogenic cytokine profiles, with blockade impacting cytokine production.

Conclusions:

  • PD-1 and Tim-3 pathways play a critical regulatory role in CD8+ T cell function during human AS.
  • Targeting PD-1 and Tim-3 may modulate immune responses relevant to AS pathogenesis.
  • Understanding these pathways offers potential therapeutic targets for atherosclerosis.