| First Author | Li Y | Year | 2017 |
| Journal | EBioMedicine | Volume | 18 |
| Pages | 188-198 | PubMed ID | 28411140 |
| Mgi Jnum | J:253209 | Mgi Id | MGI:6109039 |
| Doi | 10.1016/j.ebiom.2017.04.008 | Citation | Li Y, et al. (2017) Batf3-dependent CD8alpha(+) Dendritic Cells Aggravates Atherosclerosis via Th1 Cell Induction and Enhanced CCL5 Expression in Plaque Macrophages. EBioMedicine 18:188-198 |
| abstractText | Dendritic cells (DCs) play an important role in controlling T cell-mediated adaptive immunity in atherogenesis. However, the role of the basic leucine zipper transcription factor, ATF-like 3 (Batf3)-dependent CD8alpha(+) DC subset in atherogenesis remains unclear. Here we show that Batf3(-/-)Apoe(-/-) mice, lacking CD8alpha(+) DCs, exhibited a significant reduction in atherogenesis and T help 1 (Th1) cells compared with Apoe(-/-) controls. Then, we found that CD8alpha(+) DCs preferentially induce Th1 cells via secreting interleukin-12 (IL-12), and that the expression of interferon-gamma (IFN-gamma)or chemokine (C-C motif) ligand 5 (CCL5) in aorta were significantly decreased in Batf3(-/-)Apoe(-/-) mice. We further demonstrated that macrophages were the major CCL5-expressing cells in the plaque, which was significantly reduced in Batf3(-/-)Apoe(-/-) mice. Furthermore, we found CCL5 expression in macrophages was promoted by IFN-gamma. Finally, we showed that Batf3(-/-)Apoe(-/-) mice displayed decreased infiltration of leukocytes in the plaque. Thus, CD8alpha(+) DCs aggravated atherosclerosis, likely by inducing Th1 cell response, which promoted CCL5 expression in macrophages and increased infiltration of leukocytes and lesion inflammation. |
