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Published on: November 16, 2021
Innate and adaptive immunity in atherosclerosis
Kapka Miteva1, Rosalinda Madonna2, Raffaele De Caterina2
1Department of Biomedical Sciences, Adaptive Immunity Laboratory, Humanitas Clinical and Research Center, Rozzano, Milano, Italy.
This review details how damage-associated molecular patterns and immune cells drive atherosclerosis, a chronic inflammatory artery disease. Understanding these mechanisms, including NLRP3 inflammasome activation, is key to developing new treatments.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- Atherosclerosis is a chronic inflammatory disease affecting large and medium arteries.
- It involves subendothelial accumulation of cholesterol, immune cells, and extracellular matrix.
- Endothelial dysfunction marks the early stage of atherogenesis.
Purpose of the Study:
- To provide an overview of the atherogenesis process.
- To describe the role of damage-associated molecular patterns (DAMPs) in atherosclerosis.
- To highlight the involvement of NLRP3 inflammasome activation and immune cells in disease progression.
Main Methods:
- This is a review article, synthesizing existing research.
- It focuses on the molecular and cellular mechanisms of atherogenesis.
- Key pathways discussed include DAMPs, inflammasomes, and immune cell activation.
Main Results:
- Low-density lipoproteins can act as DAMPs, initiating inflammation.
- Innate immune cells, like monocytes and macrophages, are crucial early responders.
- Adaptive immune responses further promote atherosclerotic plaque development.
Conclusions:
- DAMPs, NLRP3 inflammasome activation, and both innate and adaptive immunity are integral to atherogenesis.
- Targeting these pathways may offer therapeutic strategies for atherosclerosis.
- Further research into immune-mediated mechanisms is warranted.
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