Journal
IMMUNITY
Volume 42, Issue 6, Pages 1100-1115Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2015.05.015
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Funding
- German Research Council [HA 1083/15-3, HA 1083/16-1, WE 2224/5-1, WE1913/11-2]
- German Centre for Cardiovascular Research (MHA VD1.2) [SFB 1123/A1, SFB 1123/Z3]
- European Research Council [AdG 249929]
- People's Republic of China
- British Heart Foundation [PG/06/083/21198, PG/12/81/29897]
- Medical Research Scotland [276 FRG-L-0806]
- Oliver Bird Studentship by Nuffield Foundation
- British Heart Foundation [PG/12/81/29897] Funding Source: researchfish
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Tertiary lymphoid organs (TLOs) emerge during non-resolving peripheral inflammation, but their impact on disease progression remains unknown. We have found in aged Apoe(-/-) mice that artery TLOs (ATLOs) controlled highly territorialized aorta T cell responses. ATLOs promoted T cell recruitment, primed CD4(+) T cells, generated CD4(+), CD8(+), T regulatory (Treg) effector and central memory cells, converted naive CD4(+) T cells into induced Treg cells, and presented antigen by an unusual set of dendritic cells and B cells. Meanwhile, vascular smooth muscle cell lymphotoxin beta receptors (VSMC-LT beta Rs) protected against atherosclerosis by maintaining structure, cellularity, and size of ATLOs though VSMC-LT beta Rs did not affect secondary lymphoid organs: Atherosclerosis was markedly exacerbated in Apoe(-/-)Ltbr(-/-) and to a similar extent in aged Apoe(-/-)Ltbr(fl/fl)Tagln-cre mice. These data support the conclusion that the immune system employs ATLOs to organize aorta T cell homeostasis during aging and that VSMC-LT beta Rs participate in atherosclerosis protection via ATLOs.
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