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The ST2 receptor (ST2L) is more prevalent in macrophages within carotid atherosclerotic plaques of symptomatic patients. This suggests the ST2L/IL-33 pathway may influence plaque development and rupture.

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Area of Science:

  • Cardiovascular Pathology
  • Immunology
  • Molecular Biology

Background:

  • ST2 (suppression of tumorigenity) functions as a receptor for interleukin-33 (IL-33), a cytokine in the IL-1 family.
  • ST2 is linked to coronary artery disease, overall mortality, and cardiovascular mortality.

Purpose of the Study:

  • To investigate the immunohistochemical expression of the ST2 receptor (ST2L) in human carotid atherosclerotic plaques.
  • To compare ST2L expression in patients with and without cerebrovascular symptoms.

Main Methods:

  • Analysis of 41 formalin-fixed paraffin-embedded internal carotid artery plaques.
  • Immunohistochemical assessment of ST2L expression in plaque cell populations.
  • Comparison of ST2L expression patterns between symptomatic and asymptomatic patient groups.

Main Results:

  • ST2L expression was significantly higher in macrophages within plaques of symptomatic patients (77.7%) compared to asymptomatic patients (39.1%).
  • ST2L expression was particularly notable in Type VI plaques (AHA classification).
  • ST2L was observed on the endothelium of neoangiogenetic vessels in plaque shoulders, but not on the endothelium of the residual lumen.

Conclusions:

  • This study provides the first large-scale investigation of ST2L immunohistochemical expression in human carotid atherosclerotic plaques.
  • ST2L expression is particularly prominent in macrophages of symptomatic patients' plaques.
  • The ST2L/IL-33 axis is hypothesized to play a role in atherosclerotic plaque development and potential rupture.