AI Article Synopsis

  • The study investigates the relationship between immune markers (PD-1, PD-L1, CD3, CD8, Foxp3) and clinical features in patients with oral leukoplakia (OLK) and oral squamous cell carcinomas (OSCC).
  • Immunohistochemical staining revealed that PD-1 expression increased in high-grade OLK, while PD-L1 was primarily found in OSCC; T cell markers were more prevalent in high-grade OLK compared to low-grade.
  • High PD-1 expression in OLK correlated with worse survival outcomes, suggesting PD-1/PD-L1 may promote immune suppression and facilitate malignant transformation in oral carcinogenesis.

Article Abstract

Objective: To evaluate the relation between the expression of PD-1, PD-L1, CD3, CD8, Foxp3 and clinicopathological features in patients with oral leukoplakia (OLK) and oral squamous cell carcinomas (OSCC) as well as the malignant outcome in OLK patients, and to study the effect of PD-1 and PD-L1 on immune microenvironment in the progression of oral carcinogenesis.

Methods: We evaluated the expression of PD-1/PD-L1 and composition of CD3 , CD8 and Foxp3 T lymphocytes in OLK and OSCC samples by immunohistochemical (IHC) staining and analyzed their relation with clinical information and malignant transformation in OLK patients.

Results: IHC staining demonstrated that the expression of PD-1 was significantly increased in the high-grade OLK group than in the low-grade OLK group, while PD-L1 was detected mainly in OSCC. The expression of CD3, CD8, and Foxp3 was found higher in the high-grade OLK group than in the low-grade OLK group, and the Foxp3 cells were found more in the OSCC group than in the high-grade OLK group. PD-1 was significantly correlated with CD3 (p < 0.05, R = 0.52), CD8 (p < 0.05, R = 0.46), and Foxp3 (p < 0.05, R = 0.46), and the low PD-1-expression group showed a better malignant-free survival than high PD-1 expression group in the OLK (p < 0.05).

Conclusion: The PD-1/PD-L1 may induce immune suppression in OLK and accelerate the progress of malignant transformation.

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Source
http://dx.doi.org/10.1111/odi.14332DOI Listing

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