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B2 cells suppress experimental abdominal aortic aneurysms.

Authors
  • Meher, Akshaya K1
  • Johnston, William F1
  • Lu, Guanyi1
  • Pope, Nicolas H1
  • Bhamidipati, Castigliano M2
  • Harmon, Daniel B3
  • Su, Gang1
  • Zhao, Yunge1
  • McNamara, Coleen A3
  • Upchurch, Gilbert R Jr4
  • Ailawadi, Gorav5
  • 1 Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Virginia, Charlottesville, Virginia.
  • 2 Department of Surgery, State University of New York Upstate Medical University, Syracuse, New York.
  • 3 Robert M. Berne Cardiovascular Research Center, Charlottesville, Virginia.
  • 4 Robert M. Berne Cardiovascular Research Center, Charlottesville, Virginia; Division of Vascular and Endovascular Surgery, University of Virginia, Charlottesville, Virginia.
  • 5 Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Virginia, Charlottesville, Virginia; Robert M. Berne Cardiovascular Research Center, Charlottesville, Virginia. Electronic address: [email protected]
Type
Published Article
Journal
American Journal Of Pathology
Publisher
Elsevier
Publication Date
November 2014
Volume
184
Issue
11
Pages
3130–3141
Identifiers
DOI: 10.1016/j.ajpath.2014.07.006
PMID: 25194661
Source
Medline
License
Unknown

Abstract

Recent reports of rupture in patients with abdominal aortic aneurysm (AAA) receiving B-cell depletion therapy highlight the importance of understanding the role of B cells (B1 and B2 subsets) in the development of AAA. We hypothesized that B2 cells aggravate experimental aneurysm formation. The IHC staining revealed infiltration of B cells in the aorta of wild-type (C57BL/6) mice at day 7 after elastase perfusion and persisted through day 21. Quantification of immune cell types using flow cytometry at day 14 showed significantly greater infiltration of mononuclear cells, including B cells (B2: 93% of total B cells) and T cells in elastase-perfused aortas compared with saline-perfused or normal aortas. muMT (mature B-cell deficient) mice were prone to AAA formation similar to wild-type mice in two different experimental AAA models. Contradicting our hypothesis, adoptive transfer of B2 cells suppressed AAA formation (102.0% ± 7.3% versus 75.2% ± 5.5%; P < 0.05) with concomitant increase in the splenic regulatory T cell (0.24% ± 0.03% versus 0.92% ± 0.23%; P < 0.05) and decrease in aortic infiltration of mononuclear cells. Our data suggest that B2 cells constitute the largest population of B cells in experimental AAA. Furthermore, B2 cells, in the absence of other B-cell subsets, increase splenic regulatory T-cell population and suppress AAA formation.

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