Verification of the expression trend and interaction prediction of innate immune cells and immune-checkpoint molecules in the process of oral mucosal carcinogenesis

Kaiyu Li ¹, Lijuan Shi ¹, Linxin Liu ¹

⁰Dept. 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.

Hua Xi Kou Qiang Yi Xue Za Zhi = Huaxi Kouqiang Yixue Zazhi = West China Journal of Stomatology +

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April 10, 2024

View abstract on PubMed

Summary

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.

Keywords:

immune checkpoint molecules immune escape immunotherapy inherent immune cells malignant transformation of oral mucosa