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Relationship Between the Proportion of CD24+ CD27+ B Cells And Lung Adenocarcinoma: Evidence From Mendelian
Peiyuan Zhong1,2, Jinhong Chen2, Tiantian Song2
1Department of Oncology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, 330006, China.
Background:
CD24+ CD27+ B cells play significant roles in multiple diseases. However, the relationship between them and Lung Adenocarcinoma (LUAD) remains elusive. This study is designed to explore the potential causal association between the proportion of CD24+ CD27+ B cells and LUAD, and to deeply understand their role in the pathogenesis of LUAD.
Methods:
Genome-Wide Association Study (GWAS) and single-cell RNA sequencing (scRNA-seq) datasets were obtained from online databases. Distinct cell subgroups were annotated using published literature. The Wilcoxon test analyzed cell infiltration proportions, and Differentially Expressed Genes (DEGs) in CD24+ CD27+ B cells between tumor and normal samples were identified. Two-Sample Mendelian Randomization (TSMR) assessed the correlation between CD24+ CD27+ B cell proportions and LUAD, as well as between DEGs and LUAD, treating these as exposure factors and LUAD as the outcome. Sensitivity analysis and MR-Steiger filtering verified results. Cell-cell communication analysis explored interactions between CD24+ CD27+ B cells and other cell types.
Results:
Nine distinct cell subgroups were identified. CD24+ CD27+ B cell proportions were significantly higher in tumors than in normal samples (P < 0.01). CD24+ CD27+ B cell proportion was a risk factor for LUAD (IVW: OR = 1.388, P = 0.032, 95% CI = 1.029-1.873). DEGs DDX24 (IVW: OR = 1.154, P = 0.013) and SCGB3A1 (IVW: OR = 1.148, P = 0.043) were also identified as risk factors. Cell-cell communication analysis revealed strong interactions between CD24+ CD27+ B cells, CD24+ CD27- B cells, and dendritic cells.
Discussion:
This study provided evidence that CD24+ CD27+ B cells were causally associated with LUAD risk, highlighting their potential role in tumor immune evasion. The identification of DDX24 and SCGB3A1 as risk genes suggested new therapeutic targets for LUAD. These findings enhanced our understanding of LUAD pathogenesis at the single-cell level and supported the development of diagnostic and immunotherapeutic strategies targeting B cell subsets.
Conclusion:
CD24+ CD27+ B cell proportion, along with DDX24 and SCGB3A1, are risk factors for LUAD, enhancing understanding at the single-cell level and supporting LUAD diagnosis and treatment.
