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Published on: February 23, 2020
Depletion of CD11c+ cell attenuates progression of abdominal aortic aneurysm
Keisuke Okuno1, Stephanie Cicalese1, Satoru Eguchi1
1Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, Pennsylvania 19140, US.A.
Insights
Depleting specific immune cells, CD11c+ dendritic cells, significantly inhibited abdominal aortic aneurysm (AAA) development in mice. This research sheds light on AAA pathogenesis and potential therapeutic targets.
Area of Science:
- Immunology
- Vascular Biology
- Pathogenesis of Aortic Aneurysms
Background:
- Chronic arterial wall inflammation is linked to abdominal aortic aneurysm (AAA) development.
- The precise molecular roles of inflammatory cells in AAA pathogenesis are not fully understood.
Purpose of the Study:
- To investigate the role of CD11c+ dendritic cells in experimental abdominal aortic aneurysm (AAA) formation.
- To elucidate the molecular mechanisms underlying AAA progression.
Main Methods:
- Experimental induction of AAA in a mouse model.
- Depletion of CD11c+ dendritic cells.
- Analysis of circulating immune cells (T cells), plasma enzyme activity, and aortic tissue remodeling.
Main Results:
- Depletion of CD11c+ dendritic cells significantly inhibited experimental AAA formation.
- Reduced levels of circulating CD4 and CD8 positive T cells were observed.
- Lowered plasma neutrophil elastase activity and altered aortic matrix remodeling were noted.
Conclusions:
- CD11c+ dendritic cells play a critical role in the pathogenesis of abdominal aortic aneurysms (AAA).
- These findings offer novel insights into AAA mechanisms and identify a potential therapeutic target for AAA formation.
Abstract:
Chronic inflammation of the arterial wall has been implicated in the development of abdominal aortic aneurysm (AAA). However, the detailed molecular mechanism(s) by which inflammatory cells contributes to AAA pathogenesis remains largely unclear. In their article in Clinical Science, Krishna et al. have reported that depletion of CD11c+ dendritic cells inhibited experimental AAA formation in mice. The authors also demonstrated a decrease in CD4 and CD8 positive T cells in the circulation, lower plasma neutrophil elastase activity, and aortic matrix remodeling. These novel findings will help clarify the underlying mechanisms of AAA progression and may provide a new target for future therapeutic research in AAA formation.
