This study investigates the causal relationship between immune cells and prostate cancer using Mendelian randomization (MR). The primary analytical method is inverse variance weighting (IVW) analysis, with comprehensive sensitivity analyses to assess heterogeneity and horizontal pleiotropy. The study identifies four immune cell traits as causally contributing to prostate cancer risk: CD127+ CD8+ T cell %CD8+ T cell, CD45RA on CD39+ resting CD4 regulatory T cell, CD62L+ Dendritic Cell Absolute Count, and CX3CR1 on CD14+ CD16+ monocyte. Additionally, two immune cell traits are identified as causally protective factors: CD4 on monocyte and FSC-A on plasmacytoid Dendritic Cell. The results provide evidence for a causal relationship between immune cells and prostate cancer, which has implications for clinical diagnosis and treatment. The study highlights the complex interplay between immune cells and prostate cancer, suggesting potential targets for immunotherapeutic interventions. However, the study acknowledges limitations, including the need for further experimental validation and the potential impact of genetic differences across populations.This study investigates the causal relationship between immune cells and prostate cancer using Mendelian randomization (MR). The primary analytical method is inverse variance weighting (IVW) analysis, with comprehensive sensitivity analyses to assess heterogeneity and horizontal pleiotropy. The study identifies four immune cell traits as causally contributing to prostate cancer risk: CD127+ CD8+ T cell %CD8+ T cell, CD45RA on CD39+ resting CD4 regulatory T cell, CD62L+ Dendritic Cell Absolute Count, and CX3CR1 on CD14+ CD16+ monocyte. Additionally, two immune cell traits are identified as causally protective factors: CD4 on monocyte and FSC-A on plasmacytoid Dendritic Cell. The results provide evidence for a causal relationship between immune cells and prostate cancer, which has implications for clinical diagnosis and treatment. The study highlights the complex interplay between immune cells and prostate cancer, suggesting potential targets for immunotherapeutic interventions. However, the study acknowledges limitations, including the need for further experimental validation and the potential impact of genetic differences across populations.