AUTHOR=Sagan Agnieszka , Mikolajczyk Tomasz P. , Mrowiecki Wojciech , MacRitchie Neil , Daly Kevin , Meldrum Alan , Migliarino Serena , Delles Christian , Urbanski Karol , Filip Grzegorz , Kapelak Boguslaw , Maffia Pasquale , Touyz Rhian , Guzik Tomasz J. 

TITLE=T Cells Are Dominant Population in Human Abdominal Aortic Aneurysms and Their Infiltration in the Perivascular Tissue Correlates With Disease Severity

JOURNAL=Frontiers in Immunology

VOLUME=10

YEAR=2019

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2019.01979

DOI=10.3389/fimmu.2019.01979

ISSN=1664-3224

ABSTRACT=<p>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 (<italic>n</italic> = 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<sup>+</sup> and CD8<sup>+</sup> T cell populations are highly activated in both compartments, with CD4<sup>+</sup> 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.</p>