View : 41 Download: 0
Indoleamine 2,3-Dioxygenase-Expressing Aortic Plasmacytoid Dendritic Cells Protect against Atherosclerosis by Induction of Regulatory T Cells
- Indoleamine 2,3-Dioxygenase-Expressing Aortic Plasmacytoid Dendritic Cells Protect against Atherosclerosis by Induction of Regulatory T Cells
- Yun T.J.; Lee J.S.; Machmach K.; Shim D.; Choi J.; Wi Y.J.; Jang H.S.; Jung I.-H.; Kim K.; Yoon W.K.; Miah M.A.; Li B.; Chang J.; Bego M.G.; Pham T.N.Q.; Loschko J.; Fritz J.H.; Krug A.B.; Lee S.-P.; Keler T.; Guimond J.V.; Haddad E.; Cohen E.A.; Sirois M.G.; El-Hamamsy I.; Colonna M.; Oh G.T.; Choi J.-H.; Cheong C.
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- Cell Metabolism
- vol. 23, no. 5, pp. 852 - 866
- Cell Press
- SCI; SCIE; SCOPUS
- Plasmacytoid dendritic cells (pDCs) are unique bone-marrow-derived cells that produce large amounts of type I interferon in response to microbial stimulation. Furthermore, pDCs also promote T cell tolerance in sterile-inflammation conditions. However, the immunomodulatory role of aortic pDCs in atherosclerosis has been poorly understood. Here, we identified functional mouse and human pDCs in the aortic intima and showed that selective, inducible pDC depletion in mice exacerbates atherosclerosis. Aortic pDCs expressed CCR9 and indoleamine 2,3-dioxygenase 1 (IDO-1), an enzyme involved in driving the generation of regulatory T cells (Tregs). As a consequence, loss of pDCs resulted in decreased numbers of Tregs and reduced IL-10 levels in the aorta. Moreover, antigen presentation by pDCs expanded antigen-specific Tregs in the atherosclerotic aorta. Notably, Tregs ablation affected pDC homeostasis in diseased aorta. Accordingly, pDCs in human atherosclerotic aortas colocalized with Tregs. Collectively, we identified a mechanism of atheroprotection mediated by tolerogenic aortic pDCs. © 2016 Elsevier Inc.
- Appears in Collections:
- 자연과학대학 > 생명과학전공 > Journal papers
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.