AI Article Synopsis

  • Abdominal Aortic Aneurysm (AAA) is linked to high cardiovascular mortality, with chronic inflammation and changes in blood vessel behavior contributing to its progression.
  • Perivascular adipose tissue (PVAT) plays a dual role, helping to maintain vascular health but also potentially promoting disease when inflamed.
  • This study found that T cells, especially activated CD4 T cells, are the dominant immune cells in AAA, particularly in PVAT, and their presence correlates with the size of the aneurysm, suggesting PVAT's significant role in AAA-related inflammation.

Article Abstract

Abdominal Aortic Aneurysm (AAA) is a major cause of cardiovascular mortality. Adverse changes in vascular phenotype act in concert with chronic inflammation to promote AAA progression. Perivascular adipose tissue (PVAT) helps maintain vascular homeostasis but when inflamed and dysfunctional, can also promote vascular pathology. Previous studies suggested that PVAT may be an important site of vascular inflammation in AAA; however, a detailed assessment of leukocyte populations in human AAA, their anatomic location in the vessel wall and correlation to AAA size remain undefined. Accordingly, we performed in depth immunophenotyping of cells infiltrating the pathologically altered perivascular tissue (PVT) and vessel wall in AAA samples at the site of maximal dilatation ( = 51 patients). Flow cytometry revealed that T cells, rather than macrophages, are the major leukocyte subset in AAA and that their greatest accumulations occur in PVT. Both CD4 and CD8 T cell populations are highly activated in both compartments, with CD4 T cells displaying the highest activation status within the AAA wall. Finally, we observed a positive relationship between T cell infiltration in PVT and AAA wall. Interestingly, only PVT T cell infiltration was strongly related to tertiles of AAA size. In summary, this study highlights an important role for PVT as a reservoir of T lymphocytes and potentially as a key site in modulating the underlying inflammation in AAA.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6736986PMC
http://dx.doi.org/10.3389/fimmu.2019.01979DOI Listing

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