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Updated: Jun 13, 2026
Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
Published on: April 22, 2019
Verification of the expression trend and interaction prediction of innate immune cells and immune-checkpoint
Kaiyu Li1, Lijuan Shi1, Linxin Liu1
1Dept. of Periodontal Mucosal Diseases, The Affiliated Stomatological Hospital, Southwest Medical University; Luzhou Key Laboratory of Oral＆Maxillofacial Reconstruction and Regeneration, Southwest Medical University, Luzhou 646000, China.
This study reveals that specific innate immune cells influence oral cancer progression by modulating immune-checkpoint molecules like CTLA4 and PD-L1. Targeting these cells offers a potential immunotherapy strategy to suppress oral mucosal carcinogenesis.
Area of Science:
- Immunology
- Oncology
- Cancer Research
Background:
- Oral mucosal carcinogenesis involves complex immune system interactions.
- Understanding the role of innate immune cells and immune-checkpoint molecules is crucial for developing effective cancer therapies.
Purpose of the Study:
- To investigate the expression trends of innate immune cells and immune-checkpoint molecules during oral mucosal carcinogenesis.
- To predict interactions between these components for potential immunotherapy strategies against oral cancer.
Main Methods:
- Utilized The Cancer Genome Atlas (TCGA) database to analyze immune cell and immune-checkpoint molecule expression.
- Collected and analyzed clinical patient blood routine data for peripheral blood immune cell assessment.
- Performed immunohistochemical and special staining to identify and validate immune cells and molecules in various stages of oral carcinogenesis.
- Conducted survival analysis to correlate immune components with oral squamous cell carcinoma prognosis.
Main Results:
- Monocytes and neutrophils expression increased, while mast cells decreased during oral carcinogenesis.
- Expression of immune-checkpoint molecules, cytotoxic T-lymphocyte-associated protein 4 (CTLA4) and programmed cell death-ligand (PD-L1), also increased.
- Monocytes, neutrophils, and eosinophils correlated positively with CTLA4 and PD-L1, potentially promoting tumor immune escape.
- Mast cells showed a negative correlation, suggesting a role in inhibiting immune escape.
Conclusions:
- Specific innate immune cell modulation can regulate CTLA4 and/or PD-L1 expression.
- Interfering with these immune cells may inhibit tumor immune escape and delay oral mucosal carcinogenesis.
- This suggests a potential immunotherapy approach for oral cancer treatment.
