Atherosclerosis--an immune disease: The Anitschkov Lecture 2007

Area of Science:

• Cardiovascular Science
• Immunology
• Pathology

Background:

• Atherosclerosis is increasingly recognized as an inflammatory disease.
• Evidence stems from patient studies, animal models, and epidemiological data.
• Immune cell involvement and inflammatory mediators are key in atherosclerotic lesions.

Purpose of the Study:

• To review the evolution of understanding atherosclerosis as an inflammatory condition.
• To highlight the role of immune cells and inflammatory markers in disease pathogenesis.
• To explore potential therapeutic avenues based on inflammatory mechanisms.

Main Methods:

• Review of studies on patients, experimental animal models, and epidemiological cohorts.
• Immunohistochemical analysis of atherosclerotic lesions.
• Cell culture experiments, clinical/epidemiological data analysis, and gene-targeted mouse studies.

Main Results:

• Immune cells (monocytes, T cells) and inflammatory mediators are integral to atherosclerotic lesions.
• Vascular cells interact with immune cells, contributing to inflammation.
• Inflammatory markers and genes are linked to myocardial infarction and stroke risk.
• Gene-targeted mouse models elucidate disease mechanisms.
• The process involves lipoprotein accumulation, endothelial activation, immune cell recruitment, foam cell formation, and T helper-1 responses.
• Regulatory immunity provides counter-regulatory anti-inflammatory signals.

Conclusions:

• Atherosclerosis pathogenesis is driven by inflammatory processes involving specific immune cells and pathways.
• Imbalance towards intensified inflammation can lead to plaque rupture, thrombosis, and ischemic events.
• Understanding the inflammatory basis of atherosclerosis opens doors for novel therapeutic strategies.