dc.description.abstract | Immunomodulatory signals regulate the self-tolerance, activation, priming and survival processes of T cells.
Programmed cell death protein 1 (PD1), Programmed death-ligand 1 (PD-L1) inhibitory signals and CD27, CD28
costimulators have been detected for many solid organ cancers in tumor-infiltrating T cells. It was aimed to
investigate the immune cell-based regulatory genetic variants in laryngeal squamous cell carcinoma (LSCC) in
terms of clinicopathological features. Genotyping was performed by PCR-RFLP method for PD-1 rs2227981, PD L1 rs2890658, CD28 rs3116496, CD27 rs2267966 genetic variants from genomic DNAs extracted from periph eral blood samples in One Hundred Thirty-Six individuals (Sixty-one LSCC and seventy-five controls). Analysis of
SNPs was carried out according to multiple inheritance models (co-dominant, dominant, recessive, over dominant and log-additive). There was no difference between LSCC and control groups in genotype/allele dis tribution for PD-1 and PD-L1 (p > 0.05). In the PD-1 overdominant model, the CT genotype was found to be high
(p = 0.036) in those without a family history. The frequency of C allele (AC+CC) in the PD-L1 dominant model
was higher in alcohol users and those with reflux (p = 0.024; p = 0.001 respectively). In the Dominant model for
PD-L1, the AA genotype was lower in moderately and well-differentiated tumors than in poorly differentiated
tumors (p = 0.02). CD27 AT and CD28 CT genotypes were found to be higher in LSCC patients compared to the
control group (p = 0.009; p = 0.01 respectively), while linkage disequilibrium (LD) was detected between CD27
and CD28 (p = 0.02). In the CD28 dominant model, C allele (CT+CC) carriage was found to be high in those with
family history and in those without reflux and perineural invasion (p = 0.01; p = 0.01; p = 0.03 respectively). In
LSCC, PD-L1 rather than PD-1 has a prognostic effect in terms of clinicopathology, and the LD and clinico pathological relationships detected between CD28 and CD27 genotypes suggest that the hereditary immune
checkpoint-dependent T cell traffic may be pathophysiologically important. | tr |