Abstract
Existing murine models of abdominal aortic aneurysms (AAAs) include pressurized intraluminal infusion of elastase, subcutaneous injection of angiotensin II in the apolipoprotein E knockout background, and periaortic application of calcium chloride. However, none of these models duplicate the periadventitial inflammation that is T helper 17 (Th17) cell dominant and might be the obstacle in developing effective strategies to prevent AAA initiation and expansion. Our previous work has demonstrated that patients with AAA have elevated plasma levels of elastin fragments, anti-elastin antibodies, and significantly elevated levels of Th17 cells sensitized to elastin degradation products (EDPs), the sum of which suggests that AAA is the result of an autoimmune response targeting elastin in the aorta.
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