T-cell immunity in acute coronary syndromes

Cornelia M. Weyand, Jörg J. Goronzy, Giovanna Liuzzo, Stephen L. Kopecky, David R. Holmes, Robert L. Frye

Research output: Contribution to journalReview articlepeer-review

74 Scopus citations


Acute coronary syndromes (ACS) are complications of atherosclerotic vascular disease that are triggered by the sudden rupture of an atheroma. Atherosclerotic plaque stability is determined by multiple factors of which immune and inflammatory pathways are critical. Unstable plaque is characterized by an infiltrate of T cells and macrophages thereby resembling a delayed hypersensitivity reaction. On activation, T cells secrete cytokines that regulate the activity of macrophages, or the T cells may differentiate into effector cells with tissue-damaging potential. Constitutive stimulation of T cells and macrophages in ACS is not limited to the vascular lesion but also involves peripheral immune cells, suggesting fundamental abnormalities in homeostatic mechanisms that control the assembly, turnover, and diversity of the immune system as a whole. This review gives particular attention to the emergence of a specialized T-cell subset, natural killer T cells, in patients with ACS. Natural killer T cells have proinflammatory properties and the capability of directly contributing to vascular injury.

Original languageEnglish (US)
Article number62486
Pages (from-to)1011-1020
Number of pages10
JournalMayo Clinic proceedings
Issue number10
StatePublished - Oct 2001


  • ACS = acute coronary syndrome
  • CAD = coronary artery disease
  • CD = cluster of differentiation
  • IFN = interferon
  • IL = interleukin
  • NK = natural killer
  • STAT = signal transducers and activators of transcription

ASJC Scopus subject areas

  • General Medicine


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