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Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro
Published on: November 26, 2018
Enhanced adhesion of monocytes via reverse signaling triggered by decoy receptor 3
Ming-Jen Hsu1, Wan-Wan Lin, Wei-Chia Tsao
1Department of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Abstract:
Decoy receptor 3 (DcR3), a newly identified soluble protein belonging to the tumor necrosis factor receptor (TNFR) superfamily, is a receptor for Fas ligand (FasL), LIGHT and TL1A. It has been demonstrated that DcR3 is frequently overexpressed by malignant tumors arising from lung, gastrointestinal tract, neuronal glia and virus-associated leukemia. Recently, we demonstrated that DcR3 is able to modulate the differentiation and activation of dendritic cells (DCs), and that DcR3-treated DCs skew naive T cell differentiation towards a Th2 phenotype. In this study, we further demonstrate that DcR3 is able to induce actin reorganization and enhance the adhesion of monocytes and THP-1 cells by activating multiple signaling molecules, such as protein kinase C (PKC), phosphatidylinositol 3-kinase (PI3K), focal adhesion kinase (FAK) and Src kinases. This provides the first evidence that the soluble DcR3, like other immobilized members of TNFR superfamily, is able to trigger 'reverse signaling' to modulate cell function.
Insights
Decoy receptor 3 (DcR3), a soluble protein, enhances monocyte adhesion by activating signaling pathways. This suggests DcR3 can trigger reverse signaling to modulate cell function.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Decoy receptor 3 (DcR3) is a soluble protein in the tumor necrosis factor receptor (TNFR) superfamily.
- DcR3 is overexpressed in various malignant tumors and associated with leukemia.
- DcR3 modulates dendritic cell (DC) differentiation and T cell responses.
Purpose of the Study:
- To investigate the role of soluble DcR3 in monocyte adhesion and actin reorganization.
- To identify the signaling pathways activated by DcR3 in monocytes.
- To explore the potential of DcR3 in triggering reverse signaling.
Main Methods:
- Treatment of monocytes and THP-1 cells with soluble DcR3.
- Analysis of actin reorganization using immunofluorescence microscopy.
- Activation of signaling molecules including protein kinase C (PKC), phosphatidylinositol 3-kinase (PI3K), focal adhesion kinase (FAK), and Src kinases.
Main Results:
- DcR3 induces significant actin reorganization in monocytes and THP-1 cells.
- DcR3 enhances the adhesion of monocytes and THP-1 cells.
- DcR3 activates key signaling molecules such as PKC, PI3K, FAK, and Src kinases.
Conclusions:
- Soluble DcR3 modulates monocyte function by inducing actin reorganization and enhancing adhesion.
- DcR3 activates multiple intracellular signaling pathways, including PKC, PI3K, FAK, and Src.
- This study provides the first evidence that soluble DcR3 can trigger reverse signaling to modulate cell function.
