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Hu, D. ; Mohanta, S.K.* ; Yin, C.* ; Peng, L.* ; Ma, Z.* ; Srikakulapu, P.* ; Grassia, G.* ; MacRitchie, N.* ; Dever, G.* ; Gordon, P.M.* ; Burton, F.L.* ; Ialenti, A.* ; Sabir, S.R.* ; McInnes, I.B.* ; Brewer, J.M.* ; Garside, P.* ; Weber, C.* ; Lehmann, T.* ; Teupser, D.* ; Habenicht, L.* ; Beer, M.* ; Grabner, R.* ; Maffia, P.* ; Weih, F.* ; Habenicht, A.J.R.*

Artery tertiary lymphoid organs control aorta immunity and protect against atherosclerosis via vascular smooth muscle cell lymphotoxin β receptors.

Immunity 42, 1100-1115 (2015)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Tertiary lymphoid organs (TLOs) emerge during nonresolving 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 β receptors (VSMC-LTβRs) protected against atherosclerosis by maintaining structure, cellularity, and size of ATLOs though VSMC-LTβRs 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-LTβRs participate in atherosclerosis protection via ATLOs.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Regulatory T-cells; E-deficient Mice; Dendritic Cells; Central Memory; Cd4(+); Inflammation; Autoimmunity; Pathogenesis; Maintenance; Recruitment
ISSN (print) / ISBN 1074-7613
e-ISSN 1097-4180
Journal Immunity
Quellenangaben Volume: 42, Issue: 6, Pages: 1100-1115 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge, Mass.
Non-patent literature Publications
Reviewing status Peer reviewed