Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:e19-e20
doi: 10.1161/01.ATV.0000199249.15199.80
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Galle, C.
Right arrow Articles by Schirmer, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Galle, C.
Right arrow Articles by Schirmer, M.
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:e19.)
© 2006 American Heart Association, Inc.


Letters to the Editor

CD8+ T-Cell Subpopulations in Human Abdominal Aortic Aneurysm Lesion

Cécile Galle

Departments of Immunology and Vascular Diseases Hôpital Erasme, Université Libre de Bruxelles Brussels, Belgium

Liliane Schandené

Department of Immunology

Jean-Pierre Dereume

Department of Vascular Diseases

Michel Goldman

Department of Immunology Hôpital Erasme, Université Libre de Bruxelles Brussels, Belgium


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

We read with interest the article by Duftner et al1 reporting the prevalence of peripheral interferon-{gamma} (IFN-{gamma})–producing CD4+CD28 and CD8+CD28 T cells in patients with small abdominal aortic aneurysm (AAA). Along with the recent description that Th1-type immune responses predominate in human end-stage AAA lesion,2,3 their observation further supports preference toward polarized type 1 T-cell responses in aneurysm disease. The potential involvement of Th1 cells in the pathogenesis of the disorder is also suggested by the convincing demonstration that absence of CD4+ T cells or targeted deletion of IFN-{gamma} prevents the induction of experimental AAA in a calcium chloride–induced mouse model,4 AAA formation being reconstituted by administration of IFN-{gamma} into CD4–/– mice or infusion of competent splenocytes from wild-type mice into IFN-{gamma}–/– mice.

In their study, Duftner et al further established that both circulating CD4+CD28 and CD8+CD28 T cells are highly differentiated cells that display extensive CD45RO to CD45RA reversion and produce large amounts of IFN-{gamma} and perforin. Surprisingly, low percentages of CD8+CD28 T cells were identified in AAA tissue sections using immunohistochemistry compared with flow cytometric analysis of peripheral blood mononuclear cells. In a series of our own, we examined the surface phenotype of infiltrating T lymphocytes freshly isolated from aneurysmal aortic wall for comparison with their circulating counterparts using flow cytometry. As shown in the Table, ex vivo immunophenotyping confirmed reduced proportions of CD8+CD28 T cells in the aneurysmal aortic wall compared with control peripheral blood. In . . . [Full Text of this Article]

Christina Duftner; Christian Dejaco; Michael Schirmer

Department of Internal Medicine Innsbruck Medical University Innsbruck, Austria