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Area of Science:

  • Immunology
  • Cardiovascular Research
  • Epigenetics

Background:

  • Monocytes and macrophages are key players in atherosclerosis.
  • The stimuli initiating monocyte activation in atherogenesis remain unclear.
  • Innate immunity was traditionally considered static, lacking memory.

Purpose of the Study:

  • To explore the role of 'trained immunity' in atherosclerosis development and progression.
  • To investigate the potential of trained immunity as a modulator of atherogenesis.
  • To identify novel therapeutic targets for atherosclerosis.

Main Methods:

  • Review of recent findings challenging the static innate immunity paradigm.
  • Examination of monocyte functional reprogramming induced by microbial products.
  • Analysis of epigenetic mechanisms, specifically histone methylation, underlying trained immunity.

Main Results:

  • Microbial product stimulation (e.g., Candida albicans) induces a long-term enhanced functional state in monocytes.
  • This 'trained immunity' involves a stronger proinflammatory response to secondary stimuli.
  • Stable histone methylation was identified as the mediating mechanism for trained immunity.

Conclusions:

  • Functional reprogramming of monocytes via trained immunity may contribute to atherogenesis.
  • Both microbial and metabolic products could induce this reprogramming.
  • Epigenetic reprogramming of monocytes is proposed as a novel therapeutic strategy for atherosclerosis.