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Circulating Th22 and Th9 levels in patients with acute coronary syndrome

Ying-zhong Lin1, Bang-wei Wu2, Zheng-de Lu1

  • 1Department of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.

Mediators of Inflammation
|January 24, 2014
PubMed

Insights

New research indicates that Th22 and Th9 cells, types of CD4+ T helper cells, may contribute to acute coronary syndromes (ACS). Increased levels of Th22 and related cytokines were observed in ACS patients, suggesting their involvement in the condition.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Cell Biology

Background:

  • CD4+ T helper (Th) cells are crucial in atherosclerosis and acute coronary syndromes (ACS).
  • Human Th cell subsets include Th1, Th2, Th17, Th22, and Th9.
  • The role of Th22 and Th9 cells in ACS onset requires further investigation.

Purpose of the Study:

  • To investigate the involvement of Th22 and Th9 cells in the onset of ACS.
  • To compare the frequencies and related molecular markers of Th22 and Th9 cells in different patient groups.

Main Methods:

  • Flow cytometry was used to detect Th22 and Th9 cell frequencies.
  • Cytokine and transcription factor levels (IL-22, AHR, IL-9, PU.1) were measured.
  • Patients with acute myocardial infarction (AMI), unstable angina pectoris (UAP), stable angina pectoris (SAP), and healthy controls were analyzed.

Main Results:

  • Peripheral Th22 cell numbers, AHR, and IL-22 levels were significantly elevated in ACS patients (AMI, UAP) compared to SAP and control groups.
  • While Th9 cell numbers did not differ, PU.1 expression and IL-9 levels were significantly increased in ACS patients versus SAP and control groups.
  • These findings suggest distinct roles for Th22 and Th9 related pathways in ACS.

Conclusions:

  • Circulating Th22 and Th9 type responses are implicated in the pathogenesis of ACS symptoms.
  • Elevated Th22 and Th9 related markers may serve as potential indicators for ACS.
  • Further research is warranted to elucidate the precise mechanisms by which these T cell subsets contribute to ACS.
Abstract

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