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Updated: Oct 23, 2025

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
Published on: January 25, 2017
Interleukin-22 promotes PD-L1 expression via STAT3 in colon cancer cells
Xiangpeng Xi1, Rui Hu2, Qi Wang3
1Department of General Surgery, The First Affiliated Hospital of Shandong First Medical University, Jinan, Shandong 250014, P.R. China.
Abstract:
Blocking the expression of programmed cell death ligand 1 (PD-L1) is a promising approach for the treatment of colon cancer. The binding of PD-L1 to its receptor programmed cell death 1 (PD-1) on immune cells leads to the apoptosis of activated T cells and causes immune escape. However, there is a limited number of patients with colon cancer that can benefit from the inhibition of PD-L1, and the regulation of PD-L1 expression is poorly understood in colon cancer. The present study demonstrated that interleukin-22 (IL-22) and PD-L1 were upregulated in colon cancer tissues and there was a positive correlation between IL-22 expression and PD-L1 expression. In the present study, exogenous IL-22 was found to upregulate PD-L1 expression via the signal transducer and activator of transcription 3 signaling pathway in human colon cancer cells (DLD-1 and primary colon cancer cells). The results of the present study revealed a novel regulatory mechanism of PD-L1 expression in colon cancer, which provides a theoretical basis for decreasing the immune tolerance of colon cancer via IL-22 overexpression.
Insights
Interleukin-22 (IL-22) upregulates programmed cell death ligand 1 (PD-L1) in colon cancer. This IL-22/PD-L1 pathway offers a new target for overcoming immune evasion in colon cancer treatment.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Programmed cell death ligand 1 (PD-L1) blockade is a cancer immunotherapy strategy.
- PD-L1 expression regulation in colon cancer is not fully understood, limiting treatment efficacy.
- Limited patient benefit from PD-L1 inhibition highlights the need for novel therapeutic targets.
Purpose of the Study:
- To investigate the role of Interleukin-22 (IL-22) in regulating PD-L1 expression in colon cancer.
- To elucidate the signaling pathway involved in IL-22-mediated PD-L1 upregulation.
- To identify new strategies for overcoming immune tolerance in colon cancer.
Main Methods:
- Analysis of PD-L1 and IL-22 expression in colon cancer tissues.
- Correlation analysis between IL-22 and PD-L1 expression levels.
- In vitro experiments using colon cancer cell lines (DLD-1 and primary cells) to assess IL-22 effects on PD-L1.
- Investigation of the signal transducer and activator of transcription 3 (STAT3) signaling pathway.
Main Results:
- Both IL-22 and PD-L1 were found to be upregulated in colon cancer tissues.
- A positive correlation was observed between IL-22 and PD-L1 expression.
- Exogenous IL-22 treatment increased PD-L1 expression in colon cancer cells.
- IL-22 upregulated PD-L1 expression through the STAT3 signaling pathway.
Conclusions:
- IL-22 is a novel regulator of PD-L1 expression in colon cancer.
- The IL-22/STAT3 pathway contributes to immune evasion in colon cancer.
- Targeting IL-22 may represent a therapeutic strategy to enhance anti-tumor immunity in colon cancer.
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