The "atheroprotective" mediators apolipoproteinA-I and Foxp3 are over-abundant in unstable carotid plaques

S. Patel*, S. H. Chung, G. White, S. Bao, D. S. Celermajer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

47 Citations (Scopus)


Objective: Inflammation is important in plaque vulnerability but the role of atheroprotective mediators in unstable plaques is not defined. The apolipoproteinA-I (apoA-I) component of HDL, and CD4+/CD25+ regulatory T cells (with their major transcription factor, Foxp3), have been implicated in the suppression of vascular inflammation. Our aim was to characterise the presence of these novel "protective" markers (apoA-I and Foxp3) in carotid plaques from symptomatic and asymptomatic subjects. Methods and results: Plaques from 57 patients (25 symptomatic, 32 asymptomatic) were stained immunohistochemically for macrophages (CD68), T cells (CD3), monocyte chemotactic protein-1 (MCP-1), matrix metalloproteinase-2 (MMP-2), myeloperoxidase (MPO), apoA-I and Foxp3. Twelve randomly selected plaques (6 asymptomatic, 6 symptomatic) were immunostained for interleukin-10 (IL-10) and interleukin-17 (IL-17). Staining was quantified using Image-Pro Plus software. Significantly greater areas of positive immunostaining for CD68, CD3, MCP-1, MMP-2, IL-17 and MPO were found in plaques from symptomatic patients compared with asymptomatic patients (p < 0.05 for all). Furthermore, significantly greater areas of positive immunostaining for apoA-I, Foxp3 and IL-10 were found in symptomatic versus asymptomatic plaques (p < 0.05 for all). The presence of apoA-I was correlated significantly and co-localised with CD3, CD68, MCP-1, MMP-2 and MPO immunostaining (R = 0.70, 0.63, 0.52, 0.55 and 0.79, respectively; p < 0.01 for all). Foxp3 immunostaining also correlated significantly with CD3 (R = 0.42), CD68 (R = 0.47), MCP-1 (R = 0.55) and MMP-2 (R = 0.44) immunostaining (p < 0.05 for all). Conclusions: ApoA-I and Foxp3 are over-abundant in plaques from symptomatic subjects and co-localise with key inflammatory mediators. These data suggest ineffective/insufficient protection against atherosclerosis-mediated inflammation by these " atheroprotective" moieties. Crown

Original languageEnglish
Pages (from-to)183-187
Number of pages5
JournalInternational Journal of Cardiology
Issue number2
Publication statusPublished - 19 Nov 2010
Externally publishedYes


  • ApolipoproteinA-I
  • Atherosclerosis
  • Foxp3
  • Inflammation
  • T cells


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