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1. Macrophang inflammatory protein 3 beta promotes survival in rat primary cortical neurons and PC12 cells | |||
MA Jun,QIAN Xiying,JIN Lide,FANG Shaolong,FU Guoping,CAO Yi,XU Wei,CAO Xia | |||
Basic Medicine 10 December 2012 | |||
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Abstract:Background We have previously reported that CCR7 may be neuroprotective in the central nervous system. This study aimed to investigate whether macrophage inflammatory protein 3 beta (MIP-3 beta /CCL19), which is the ligand for CCR7, could promote survival in primary neurons and PC12 cells in vitro. Results We found that within the concentration range of 50 to 200 ng/ml, MIP-3 beta promoted survival in serum-deprived rat primary cortical neurons as well as reduced serum deprivation-induced Bim expression. However, primary cortical neurons were less viable at higher concentrations of MIP-3 beta (≥300 ng/ml). To investigate whether MIP-3 beta acts through its receptor, CCR7, the pEGFP-N1-CCR7 expression vector was constructed and transfected into PC12 cells. We found that MIP-3 beta enhanced survival of PC12 cells that were transfected with pEGFP-N1-CCR7 in serum-free media. In these transfected PC12 cells, MIP-3 beta increased Akt phosphorylation levels at 15 and 60 min this effect was effectively blocked by wortmannin, a specific PI3K inhibitor. ConclusionsThese data suggest that MIP-3 beta promotes survival in serum-deprived rat primary cortical neurons through its receptor, CCR7, and acts as a neurotrophic factor in PC12 cells, most likely via the PI3K/Akt signaling pathway. | |||
TO cite this article:MA Jun,QIAN Xiying,JIN Lide, et al. Macrophang inflammatory protein 3 beta promotes survival in rat primary cortical neurons and PC12 cells[OL].[10 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4500497 |
2. 4-1BBL reverse signaling potently induces Dendritic Cells development from human monocytes | |||
Songguang Ju,Songwen Ju,Xueguang Zhang | |||
Basic Medicine 08 January 2009 | |||
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Abstract:Dendritic cells (DCs) are responsible for the initiation of immune responses. Our study demonstrates a new pathway for generating a large quantity of stimulatory monocyte derived DCs (Mo-DCs) from human monocytes using anti-4-1BB Ligand (4-1BBL) mAb to trigger reverse signaling. The anti-4-1BBL-driven-Mo-DCs (DCsα-4-1BBL) not only express higher levels of CD86, CD83 and HLA-DR, when compared to the Mo-DCs matured by TNF-α, they also exhibit a unique phenotype that expresses lower levels of PD-L1. High levels of GM-CSF, M-CSF, and Flt3 Ligand(FL) were found in the anti-4-1BBL-differentiation culture. Neutralizing M-CSF, GM-CSF, and FL inhibited Mo-DC proliferation stimulated by anti-4-1BBL mAb, suggesting that M-CSF, GM-CSF, and FL are involved in cell proliferation stimulated by anti-4-1BBL. Further analysis of the DCsα-4-1BBL showed increased secretion of Th1-type cytokines IL-12 and IFN-γ, and decreased secretion of IL-10. DCsα-4-1BBL induced much stronger proliferative responses in the MLR assay when compared with DCs derived by GM-CSF. Moreover, DCsα-4-1BBL preferentially induced Th1 responses. We have further demonstrated that anti-4-1BBL antibody stimulated nuclear translocation of NF-κB from the cytoplasm in monocytes, suggesting reverse signaling by 4-1BBL is likely responsible for mediating DCs differentiation. Collectively, we have found that reverse signaling of 4-1BBL promotes the differentiation of potent Th1-inducing DCs from human monocytes. | |||
TO cite this article:Songguang Ju,Songwen Ju,Xueguang Zhang. 4-1BBL reverse signaling potently induces Dendritic Cells development from human monocytes[J]. |
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