Aneurysmal lesions of patients with abdominal aortic aneurysm contain clonally expanded T cells

• Published in: The Journal of immunology (1950) Vol. 192; no. 10; pp. 4897 - 4912
• Main Authors: Lu, Song, White, John V, Lin, Wan Lu, Zhang, Xiaoying, Solomides, Charalambos, Evans, Kyle, Ntaoula, Nectaria, Nwaneshiudu, Ifeyinwa, Gaughan, John, Monos, Dimitri S, Oleszak, Emilia L, Platsoucas, Chris D
• Format: Journal Article
• Language: English
• Published: United States AAI 15-05-2014
• Subjects: Aged; Aged, 80 and over; Aortic Aneurysm, Abdominal - immunology; Aortic Aneurysm, Abdominal - pathology; Cell Proliferation; Clonal Selection, Antigen-Mediated; Female; Humans; Male; Middle Aged; Molecular and Structural Immunology; Receptors, Antigen, T-Cell, alpha-beta - immunology; T-Lymphocytes - immunology; T-Lymphocytes - pathology
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.1301009

Abdominal aortic aneurysm (AAA) is a common disease with often life-threatening consequences. This vascular disorder is responsible for 1-2% of all deaths in men aged 65 years or older. Autoimmunity may be responsible for the pathogenesis of AAA. Although it is well documented that infiltrating T cells are essentially always present in AAA lesions, little is known about their role in the initiation and/or progression of the disease. To determine whether T cells infiltrating AAA lesions contain clonally expanded populations of T cells, we amplified β-chain TCR transcripts by the nonpalindromic adaptor-PCR/Vβ-specific PCR and/or Vβ-specific PCR, followed by cloning and sequencing. We report in this article that aortic abdominal aneurysmal lesions from 8 of 10 patients with AAA contained oligoclonal populations of T cells. Multiple identical copies of β-chain TCR transcripts were identified in these patients. These clonal expansions are statistically significant. These results demonstrate that αβ TCR(+) T lymphocytes infiltrating aneurysmal lesions of patients with AAA have undergone proliferation and clonal expansion in vivo at the site of the aneurysmal lesion, in response to unidentified self- or nonself Ags. This evidence supports the hypothesis that AAA is a specific Ag-driven T cell disease.