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Author Spotlight: Advancing Treatment Approaches with Adipose-Derived Stem Cells
Published on: January 12, 2024
Roles of PD-L1 in human adipose-derived mesenchymal stem cells under inflammatory microenvironment
Jinqiu Sun1, Hannah Zhong2, Bo Kang3
1Institute of Life Science and Green Development, College of Life Sciences, Hebei University, Baoding, China.
Abstract:
Mesenchymal stem cells (MSCs) display unique homing and immunosuppression features which make them promising candidates for cell therapy in inflammatory disorders. It is known that C-X-C chemokine receptor type 4 (CXCR4, also known as CD184) is a critical receptor implicated in MSCs migration, and the protein programmed death ligand-1 (PD-L1) is involved in MSC's immunosuppression. However, it remains unclear how the molecular mechanisms regulate PD-L1 expression for migration and immunosuppression of MSCs under the inflammatory microenvironment. In this article, we used the human adipose-derived mesenchymal stem cells (hADMSCs) treated with lipopolysaccharide (LPS) as an in vitro inflammatory model to explore the roles of PD-L1 on the migration and immunosuppression of MSC. Our results demonstrate that in hADMSCs, LPS significantly increased PD-L1 expression, which mediated the migration of the LPS-treated hADMSCs via CXCR4. In addition, we found that the increased PD-L1 expression in the LPS-treated hADMSCs inhibited B cell proliferation and immunoglobulin G secretion through nuclear factor-κB. Our study suggests that the PD-L1 plays critical roles in the homing and immunosuppression of MSCs which are a promising cell therapy to treat inflammatory diseases.
Insights
Mesenchymal stem cells (MSCs) migration and immunosuppression are regulated by programmed death ligand-1 (PD-L1) via CXCR4 in inflammation. PD-L1 mediates MSC homing and inhibits B cell activity, highlighting its therapeutic potential for inflammatory diseases.
Area of Science:
- Immunology
- Cell Biology
- Regenerative Medicine
Background:
- Mesenchymal stem cells (MSCs) show promise for treating inflammatory disorders due to their homing and immunosuppressive properties.
- C-X-C chemokine receptor type 4 (CXCR4) is crucial for MSC migration, and programmed death ligand-1 (PD-L1) mediates immunosuppression.
- The regulation of PD-L1 expression in MSCs within inflammatory environments remains incompletely understood.
Purpose of the Study:
- To investigate the role of PD-L1 in the migration and immunosuppression of human adipose-derived mesenchymal stem cells (hADMSCs) under inflammatory conditions.
- To elucidate the molecular mechanisms linking PD-L1 expression to MSC function in an inflammatory microenvironment.
Main Methods:
- Utilized lipopolysaccharide (LPS) to establish an in vitro inflammatory model using hADMSCs.
- Assessed the impact of LPS on PD-L1 expression and its correlation with MSC migration via CXCR4.
- Evaluated the effect of increased PD-L1 on B cell proliferation and immunoglobulin G secretion, investigating the role of nuclear factor-κB (NF-κB).
Main Results:
- LPS treatment significantly upregulated PD-L1 expression in hADMSCs.
- Upregulated PD-L1 mediated the migration of LPS-treated hADMSCs, involving CXCR4.
- Increased PD-L1 expression in hADMSCs suppressed B cell proliferation and immunoglobulin G secretion through NF-κB signaling.
Conclusions:
- PD-L1 plays a critical role in mediating the homing and immunosuppressive functions of MSCs in inflammatory settings.
- The PD-L1/CXCR4 axis is essential for MSC migration under inflammation.
- Targeting PD-L1 may enhance the therapeutic efficacy of MSCs for inflammatory diseases.
