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Research progress on Th17 and T regulatory cells and their cytokines in regulating atherosclerosis

Qiong Wang1, Yurong Wang1, Danyan Xu2

  • 1Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, China.

Frontiers in Cardiovascular Medicine
|October 10, 2022
PubMed

Insights

Immune cells like helper T17 (Th17) and regulatory T cells (Tregs) significantly impact atherosclerosis. Imbalances in Th17/Treg cells and their associated cytokines, such as IL-17, influence disease progression and plaque stability.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Inflammation Biology

Background:

  • Atherosclerosis, a primary cause of coronary heart disease, is characterized by chronic arterial wall inflammation.
  • Immune cells critically influence the inflammatory processes driving atherosclerosis progression and outcomes.

Purpose of the Study:

  • To review the mechanisms of CD4+ T cell subsets, specifically helper T17 (Th17) cells and regulatory T cells (Tregs), in regulating atherosclerosis.
  • To focus on the roles of interleukin-17 (IL-17), IL-10, and other cytokines in atherosclerosis and the factors affecting their influence.

Main Methods:

  • Literature review of immunological mechanisms in atherosclerosis.
  • Analysis of the interplay between Th17 cells, Tregs, and cytokine profiles.
  • Examination of factors modulating cytokine effects in the context of atherosclerosis.

Main Results:

  • Interleukin-17 (IL-17), secreted by Th17 cells, can promote atherosclerosis but may also stabilize plaques.
  • Regulatory T cells (Tregs) exhibit a protective role in atherosclerosis.
  • An imbalance between Th17 and Treg cells is significantly implicated in atherosclerosis pathogenesis.

Conclusions:

  • Immune responses are crucial regulators of atherosclerosis.
  • Understanding immune cell mechanisms offers potential therapeutic targets for atherosclerosis.
  • Further research is essential to fully elucidate these mechanisms and support clinical drug development.
Abstract

Keywords:
CD4+ T cellsIL-17Th17/Treg balanceTregsatherosclerosis

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