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Citation
Tags
HERO ID
7144626
Reference Type
Journal Article
Title
Artery tertiary lymphoid organs contribute to innate and adaptive immune responses in advanced mouse atherosclerosis
Author(s)
Mohanta, SK; Yin, C; Peng, L; Srikakulapu, P; Bontha, V; Hu, D; Weih, F; Weber, C; Gerdes, N; Habenicht, AJ; ,
Year
2014
Is Peer Reviewed?
Yes
Journal
Circulation Research
ISSN:
0009-7330
EISSN:
1524-4571
Language
English
PMID
24855201
DOI
10.1161/CIRCRESAHA.114.301137
Abstract
Tertiary lymphoid organs emerge in tissues in response to nonresolving inflammation. Recent research characterized artery tertiary lymphoid organs in the aorta adventitia of aged apolipoprotein E-deficient mice. The atherosclerosis-associated lymphocyte aggregates are organized into distinct compartments, including separate T-cell areas harboring conventional, monocyte-derived, lymphoid, and plasmacytoid dendritic cells, as well as activated T-cell effectors and memory cells; B-cell follicles containing follicular dendritic cells in activated germinal centers; and peripheral niches of plasma cells. Artery tertiary lymphoid organs show marked neoangiogenesis, aberrant lymphangiogenesis, and extensive induction of high endothelial venules. Moreover, newly formed lymph node-like conduits connect the external lamina with high endothelial venules in T-cell areas and also extend into germinal centers. Mouse artery tertiary lymphoid organs recruit large numbers of naïve T cells and harbor lymphocyte subsets with opposing activities, including CD4(+) and CD8(+) effector and memory T cells, natural and induced CD4(+) regulatory T cells, and memory B cells at different stages of differentiation. These data suggest that artery tertiary lymphoid organs participate in primary immune responses and organize T- and B-cell autoimmune responses in advanced atherosclerosis. In this review, we discuss the novel concept that pro- and antiatherogenic immune responses toward unknown arterial wall-derived autoantigens may be organized by artery tertiary lymphoid organs and that disruption of the balance between pro- and antiatherogenic immune cell subsets may trigger clinically overt atherosclerosis.
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