Increased Th17 cell frequency concomitant with decreased Foxp3+ Treg cell frequency in the peripheral circulation of patients with carotid artery plaques

Inflamm Res. 2012 Oct;61(10):1155-65. doi: 10.1007/s00011-012-0510-2. Epub 2012 Jun 23.

Abstract

Objective and design: We investigated a possible imbalance between T helper (Th)17 and CD4+ CD25+ forkhead/winged helix transcription factor (Foxp3) T regulatory (Treg) cells in patients with carotid artery plaques.

Material or subjects: From November 2009 to September 2010, we enrolled 126 males and 104 females with mean age 68.24 ± 6.71 years.

Treatment: Based on carotid artery sonography, the 230 subjects were categorized into three groups: plaque negative; stable plaques; and unstable plaques.

Methods: Th17 and Treg cell frequencies, relevant plasma cytokines (IL-17, IL-6, IL-23, and TNF-α), and RORγt mRNA levels were determined.

Results: Compared to plaque negative, Th17 cells, Th17-related cytokines (IL-17, IL-6, IL-23, and TNF-α), and RORγt mRNA levels were higher with stable plaques, and highest with unstable plaques. The opposite trend was found for Treg cells, Treg-related cytokines (IL-10 and TGF-β1), and Foxp3 mRNA. Th17 cell frequencies were significantly negatively correlated with Treg cell frequencies.

Conclusions: Our investigation demonstrated that there is a Th17/Treg functional imbalance in patients with unstable carotid atherosclerotic plaques. Th17 cells may promote atherogenesis, while Treg cells may have a protective role against atherosclerosis plaques. An imbalance of Th17/Treg cells may offer a new direction for the treatment of atherosclerosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Carotid Stenosis / blood
  • Carotid Stenosis / genetics
  • Carotid Stenosis / immunology*
  • Cells, Cultured
  • Chemokine CCL2 / genetics
  • Cytokines / blood
  • Female
  • Forkhead Transcription Factors / genetics*
  • Humans
  • Leukocytes, Mononuclear / cytology
  • Male
  • Middle Aged
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / genetics
  • RNA, Messenger / metabolism
  • T-Lymphocytes, Regulatory / immunology*
  • Th17 Cells / immunology*

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • Cytokines
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Nuclear Receptor Subfamily 1, Group F, Member 3
  • RNA, Messenger
  • RORC protein, human