Related Experiment Video
Updated: Mar 23, 2026

Quantifying Antibody-Dependent Cellular Cytotoxicity in a Tumor Spheroid Model: Application for Drug Discovery
Published on: April 26, 2024
[Sunitinib inhibits the expressions of co-stimulatory molecule ligands on dendritic cells]
Chao Ding1, Haixing Mai2, Lijun Chen3
1Department of Urology, Clinical College, No. 307 Hospital of PLA, Anhui Medical University, Beijing 100071, China.
Objective:
To investigate the effect of sunitinib on the expressions of co-stimulatory molecule ligands, programmed death ligand 1 (PD-L1), PD-L2, CD80, CD86, B7-H4 and herpes virus entry mediator (HVEM) on peripheral blood monocyte-derived dendritic cells (DCs) from patients with renal cell carcinoma (RCC).
Methods:
Monocyte-derived DCs from patients with RCC were cultured in vitro and randomly divided into three groups: sunitinib combined with lipopolysaccharide (LPS), LPS only and dimethyl sulfoxide (DMSO) treatment. Sunitinib plus LPS group was pretreated with 200 ng/mL sunitinib for 12 hours followed by stimulated with 1 μg/mL LPS for 24 hours; LPS group was pretreated with 1 μL/mL DMSO for 12 hours and then stimulated with 1 μg/mL LPS for 24 hours; DMSO group was treated with 1 μL/mL DMSO for 36 hours. Morphological changes were observed by an inverted microscope. Flow cytometry was used to detect the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM.
Results:
Sunitinib-LPS co-treated and LPS-treated cells had typical dendrites, while DMSO-treated cells had no obvious dendrites. Compared with the LPS-treated group, the expressions of CD80, PD-L1 and B7-H4 on DCs significantly decreased in the sunitinib-LPS group; the expressions of PD-L1, PD-L2, CD80, CD86, B7-H4 and HVEM were lower in the DMSO group.
Conclusion:
Sunitinib inhibits the expressions of CD80, PD-L1 and B7-H4 on DCs induced by LPS.
Insights
Sunitinib treatment reduces key immune checkpoint ligands, programmed death ligand 1 (PD-L1) and B7-H4, on dendritic cells (DCs) from renal cell carcinoma patients. This suggests sunitinib may modulate immune responses in RCC.
Area of Science:
- Immunology
- Oncology
- Pharmacology
Background:
- Renal cell carcinoma (RCC) is a significant malignancy.
- Dendritic cells (DCs) play a crucial role in immune regulation.
- Immune checkpoint molecules, such as PD-L1, are implicated in cancer immune evasion.
Purpose of the Study:
- To evaluate the impact of sunitinib on co-stimulatory molecule ligand expression.
- To investigate sunitinib's effect on programmed death ligand 1 (PD-L1), PD-L2, CD80, CD86, B7-H4, and HVEM.
- To assess these changes on monocyte-derived dendritic cells (DCs) from RCC patients.
Main Methods:
- Monocyte-derived DCs from RCC patients were cultured in vitro.
- Cells were treated with sunitinib plus lipopolysaccharide (LPS), LPS alone, or dimethyl sulfoxide (DMSO).
- Flow cytometry was employed to quantify the expression of target molecules.
Main Results:
- Sunitinib-LPS co-treatment and LPS-only treatment induced typical dendritic cell morphology.
- Compared to LPS treatment alone, sunitinib significantly decreased CD80, PD-L1, and B7-H4 expression on DCs.
- The DMSO-treated group showed lower expression of PD-L1, PD-L2, CD80, CD86, B7-H4, and HVEM.
Conclusions:
- Sunitinib inhibits the LPS-induced expression of CD80, PD-L1, and B7-H4 on dendritic cells.
- These findings suggest a potential mechanism by which sunitinib may modulate the tumor immune microenvironment in RCC.
More Related Videos
Related Concept Videos
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Inhibition of Cdk Activity
Inhibition of CDK Activity
The JAK-STAT Signaling Pathway
Tumor Immunotherapy

