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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 möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter 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
Zeitschrift Immunity
Quellenangaben Band: 42, Heft: 6, Seiten: 1100-1115 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed