Key result
Medial vascular smooth muscle cells potentially coordinate crosstalk between adventitial inflammation and intimal atherosclerosis.
Why the study?
The relevance and impact of adventitial inflammation, specifically adventitial tertiary lymphoid organs, on atherogenesis and their interaction with intimal atherosclerotic lesions remain to be fully elucidated.
This review highlights the role of adventitial tertiary lymphoid organs (ATLOs) and their interaction with intimal atherosclerotic lesions in atherogenesis.
ATLOs in atherosclerotic mice may modulate plaque inflammation; leaves open their causal role and therapeutic targeting in humans.
The presence of adventitial inflammation in correlation with atherosclerotic lesions has been recognized for decades. In the last years, several studies have investigated the relevance and impact of adventitial inflammation on atherogenesis. In the abdominal aorta of elderly Apoe(-/-) mice, adventitial inflammatory structures were characterized as organized ectopic lymphoid tissue, and therefore termed adventitial tertiary lymphoid organs (ATLOs). These ATLOs possess similarities in development, structure and function to secondary lymphoid organs. A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process. We here review the development, phenotypic characteristics, and function of ATLOs in atherosclerosis. Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.
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Akhavanpoor et al. (2014) conducted a review in Atherosclerosis. Adventitial inflammation and tertiary lymphoid organs was evaluated. Adventitial inflammation and tertiary lymphoid organs interact with intimal atherosclerotic lesions, a crosstalk potentially coordinated by medial vascular smooth muscle cells.
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