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Exogenous dendritic cells aggravate atherosclerosis via P-selectin/ PSGL-1 pathway


1 Department of Cardiology, The First Affiliated Hospital of Dalian Medical University, Dalian, 116011, China
2 Cardiac Center/Division of Cardiovascular Diseases, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China
3 Dalian Medical University, Dalian Medical University, Dalian, 116044, China

* Address correspondence to: Rongchong Huang,

BIOCELL 2020, 44(2), 225-236.


Studies have found that a large number of inflammatory cells, P-selectin, and mature dendritic cells (DCs) are expressed in the damaged and shoulder parts of atherosclerotic plaque, which demonstrates that P-selectin and mature DCs participate in the immune inflammatory response leading to the development of atherosclerosis. However, it is unclear how the above factors interact in this setting. In this study, we investigated the role of P-selectin and its receptor, P-selectin glycoprotein ligand (PSGL)-1 in atherosclerosis, with the finding that DC surface marker expression was consistently high in the P-selectin group while consistently low in the PGSL-1 + DCs group, with CD40 and CD86 expressed by 3.84% and 2.05% for the latter. The highest expression of CD80, CD83, and MHC II was discovered in the DC group, at 7.49%, 3.68%, and 8.98%, respectively. Results of this study are similar to those obtained previously by Ye et al. (2017), which showed larger atherosclerotic lesions in mice that received exogenous DCs, compared with those treated with PBS. In this study, the greatest level of atherosclerosis, fibrosis, and lipid deposition was also seen in mice that received exogenous DCs.


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ZHONG, L., GUO, L., YE, Z., ZHANG, S., HUANG, R. (2020). Exogenous dendritic cells aggravate atherosclerosis via P-selectin/ PSGL-1 pathway. BIOCELL, 44(2), 225–236.

This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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