The Th17/Treg imbalance exists in patients with heart failure with normal ejection fraction and heart failure with

Na Li1, Hongjun Bian, Juan Zhang

  • 1The Key Laboratory of Cardiovascular Remodeling and Function Research of Chinese Ministry of Education and Public Health, Shandong University Qilu Hospital, 250012 Jinan, Shandong Province, China.

Insights

Chronic heart failure (CHF) is linked to an imbalance between T helper 17 (Th17) cells and regulatory T (Treg) cells. This study found higher Th17 and lower Treg frequencies in CHF patients, suggesting a potential therapeutic target.

Area of Science:

  • Immunology
  • Cardiology
  • Inflammation research

Background:

  • Immune activation and inflammation are key drivers in chronic heart failure (CHF) progression.
  • T helper (Th) lymphocytes, specifically Th17 and regulatory T (Treg) cells, play critical roles in immune regulation.
  • The balance between Th17 and Treg cells is crucial for controlling inflammation and autoimmune responses.

Purpose of the Study:

  • To investigate the hypothesis that the Th17/Treg cell balance is disrupted in patients with chronic heart failure (CHF).
  • To compare Th17 and Treg cell frequencies in different subgroups of CHF patients and healthy controls.

Main Methods:

  • Patients with CHF were categorized into two groups: heart failure with normal ejection fraction (HFNEF) and heart failure with reduced ejection fraction (HFREF).
  • Peripheral blood samples were analyzed using flow cytometry to quantify the frequencies of Th17 and Treg cells.

Main Results:

  • Both HFNEF and HFREF patient groups exhibited a significant increase in Th17 cell frequencies compared to control groups.
  • A notable decrease in Treg cell frequencies was observed in both HFNEF and HFREF patients relative to controls.

Conclusions:

  • The findings confirm a Th17/Treg cell imbalance in patients suffering from CHF.
  • This immune dysregulation may contribute to the pathogenesis of CHF.
  • Restoring the Th17/Treg balance presents a potential therapeutic strategy for managing CHF.
Abstract

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