IMR Press / FBL / Volume 19 / Issue 3 / DOI: 10.2741/4226

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Effects of rapamycin on DC-SIGN expression and biological functions in DC
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1 Department of Pediatrics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
2 Department of Nephrology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
3 Shanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai JiaoTong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China
4 State Key Laboratory of Medical Genomics and Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, China
Academic Editor:Tong Zhou
Front. Biosci. (Landmark Ed) 2014, 19(3), 557–565; https://doi.org/10.2741/4226
Published: 1 January 2014
(This article belongs to the Special Issue Immune pathology)
Abstract

Rapamycin, a macrolide antibiotic, has potent immunosuppressive properties as an antirejection therapy in organ transplantation. Studies show that dendritic cells (DC) are important targets for rapamycin, which can inhibit DC maturation and DC-induced allogeneic T cell proliferation. In this study, we investigated the effects of rapamycin on the expressions of DC-SIGN and transcription factor PU.1 and the function of DC. Treatment with rapamycin significantly reduced the expression of DC-SIGN in a dose-dependent manner associated with suppression of PU.1 gene expression and the ability of DC to migrate and stimulate T cell proliferation. The expression of DC-SIGN was significantly suppressed using PU.1 siRNA. Intriguingly, rapamycin treatment largely decreased the expressions of PU.1 and DC-SIGN in THP-1 cells. In addition, treatment with rapamycin down-regulated the promoter activity of DC-SIGN. In conclusion, rapamycin inhibits DC-SIGN expression and suppresses the ability of DC to migrate and stimulate T cell proliferation through the PU.1 gene transcription pathway.

Keywords
Rapamycin
DC-SIGN
dendritic cell
transcription factor PU.1
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