ArticleJournal of the American Heart Association2025
Unraveling Novel Subsets of Lymphocytes Involved in Sac Expansion in the Tertiary Lymphoid Structure Within an Abdominal Aortic Aneurysm.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The Inflammation-Thrombosis Genetic Axis in Abdominal Aortic Aneurysm: A Shared Roadmap to Precision Medicine.TH open : companion journal to thrombosis and haemostasis · 2026Review
- Complement and diverse enrichment of antibodies in intraluminal thrombi from abdominal aortic aneurysms may contribute to increased inflammation.Scientific reports · 2025Article
- Identification of ARHGAP9 as a Key Diagnostic Marker for Abdominal Aortic Aneurysm by Multiomics and Experimental Validation.Human mutation · 2025Article
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Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic inflammation is involved in the development of abdominal aortic aneurysm (AAA). A tertiary lymphoid structure (TLS) within vascular lesions has recently been focused on for its role in modulation of inflammation in local tissues. We aimed to elucidate the relationships between TLS and pathophysiology of AAA.
methodsAbdominal aortic samples obtained from 37 patients with AAA (men/women: 34/3, age: 72.8±9.9 years) and 15 autopsied patients who died from non-aortic events (men/women: 11/4, age: 65.5±9.8 years) were investigated.
resultsTLSs in AAA lesions were confirmed by focal infiltration of CD3-positive cells surrounding germinal center-like structures containing CD20-positive cells between the tunica adventitia and tunica media layers. The formation of a TLS was significantly more prevalent in AAA patients than in autopsied patients. The number of TLSs in AAA lesions was positively correlated with sac diameter (r=0.357,
conclusionsThe formation of a TLS in AAA lesions is associated with sac diameter and intraluminal thrombosis in connection with interfollicular T follicular helper cells and double negative B cells, which may contribute to the pathophysiology of AAA and might be novel therapeutic targets for the development of AAA.
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