Supporting data for "Tumor-derived CCL20 drives B cell dysfunction and immunosuppression in nasopharyngeal carcinoma"

The raw data supporting the findings of ‘Tumor-derived CCL20 Drives B Cell Dysfunction and Immunosuppression in Nasopharyngeal Carcinoma’ encompass RNA-sequencing datasets, bioinformatic analyses, flow cytometry, and multiplex immunohistochemistry (mIHC) staining results, among other experimental outputs.Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus-associated malignancy with a B cell-rich microenvironment, the role of tumor factors in shaping B cell immune responses remains poorly understood. Multi-omics analysis of NPC patient specimens revealed that memory B cell infiltration correlates with favorable clinical outcomes. We found that tumor-derived CCL20 drives B cell dysfunction through CCR6-dependent suppression of BCR/AKT signaling, leading to diminished expression of activation markers (CD80/CD86/MHC-II) and impaired memory differentiation via CD27 downregulation. This CCL20-induced "paralyzed" state compromises B cell antigen presentation capacity, resulting in defective CD4+ and CD8+ T cell activation and attenuated cytotoxic responses. Multiplex immunohistochemistry confirmed an inverse relationship between tumor CCL20 levels and both memory B cell frequency and MHC-I expression on CD20+ B cells. Spatial transcriptomic profiling further demonstrated that CCL20-enriched tumor regions colocalize with malignant epithelial cells, exhibit reduced CD4+ T cell infiltration, and display transcriptional suppression of B cell lineage markers (MS4A1/CD20, CD19, CD27, IGHD) and MHC molecules. Collectively, these findings establish that tumor-secreted CCL20 fosters an immunosuppressive niche by paralyzing B cell function, disrupting memory formation, and impairing T cell priming. The CCL20-CCR6 axis represents a therapeutic target to restore antitumor immunity, with CCL20 serving as both a prognostic biomarker and immunotherapeutic intervention point in NPC.