IL-23 as a potential mediator of immune evasion and therapeutic target in laryngeal squamous cell carcinoma

Laryngeal squamous cell carcinoma (LSCC) is a prevalent and aggressive malignancy. Interleukin-23 (IL-23) and its receptor (IL-23R) have been identified as key modulators of the immune response in various cancers, but their role in LSCC remains unclear. This study aimed to examine the expression of IL-23, IL-23R, and FoxP3 + regulatory T cells (Tregs) in LSCC tissues and explore their potential involvement in immune modulation and tumor progression. Immunohistochemical staining was performed on 115 LSCC tissue samples to assess the expression of IL-23, IL-23R, and FoxP3 + Tregs. The relationship between IL-23 expression and immune cell infiltration, including CD8 + T cells and Tregs, was analyzed, and survival analysis was conducted. Public datasets (TCGA-HNSC, GSE103322) were utilized for bioinformatic validation. IL-23 was predominantly expressed in tumor cells and stromal immune cells within the TME, while IL-23R was primarily located on immune cells, especially in the invasive margin. IL-23 expression was positively correlated with Treg infiltration and negatively associated with CD8 + T cell density. However, no significant correlation was found between IL-23 expression and overall survival, potentially due to the study’s sample size limitations. Bioinformatic analysis of the TCGA-HNSC cohort confirmed elevated IL23A expression in tumors and revealed its positive correlation with immune infiltration scores, Treg signatures, and enrichment in immune-related pathways. IL-23, through its interaction with IL-23R and Tregs, contributes to immune evasion in LSCC. Targeting the IL-23/IL-23R signaling axis may offer a novel therapeutic approach to enhance anti-tumor immunity in LSCC. Larger cohort studies are needed to validate these findings and assess IL-23’s clinical utility as a biomarker and therapeutic target.