Immune-mediated mechanisms in atherosclerosis: Prevention and treatment of clinical manifestations

A. Niessner, J. J. Goronzy, C. M. Weyand

Research output: Contribution to journalReview articlepeer-review

15 Scopus citations


Accumulation of inflammatory cells identifies atherosclerotic plaque at risk for rupture. Typically, activated immune cells occupy the rupture-prone areas of the atherosclerotic lesion. These cells are an appealing therapeutic target for novel strategies of plaque stabilization. Biologic consequences of plaque inflammation ultimately depend not only on the cellular players populating the lesion but also on triggers of immune activation originating from within the plaque or arriving from the circulation, and immune effector mechanisms that mediate cellular damage and plaque destabilization. Recent studies have provided insights into particular immune mechanisms in the atherosclerotic plaque that contribute to plaque vulnerability. This knowledge provides the basis for potential immunomodulatory therapies in cardiovascular disease. These therapeutic approaches can be classified as (1) immunomodulatory effects of existing therapies, (2) therapies targeting inflammatory triggers, and (3) agents inhibiting specific immune mechanisms.

Original languageEnglish (US)
Pages (from-to)3701-3710
Number of pages10
JournalCurrent pharmaceutical design
Issue number36
StatePublished - Dec 2007


  • Atherosclerosis
  • Cardiovascular disease
  • Immune mechanisms
  • Immunomodulatory therapies
  • Inflammation
  • Plaque

ASJC Scopus subject areas

  • Pharmacology
  • Drug Discovery


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