慢性非细菌性前列腺炎（CNP）发病率高，治疗后易复发，严重影响患者生活质量，目前机制尚未阐明。研究发现Th1细胞局部浸润可导致CNP发生。前期基于非细菌性前列腺炎动物模型组织测序鉴定并验证出一关键CXCL12/CXCR4轴，其可通过调控淋巴细胞趋化介导CNP发生。文献报道CXCR4蛋白可激活LASP1/AKT通路促进炎症细胞迁移，但具体机制不明。基于预实验结果和文献报道，我们推测“CXCL12/CXCR4轴可通过激活LASP1/AKT信号通路促进Th1细胞迁移至前列腺，引起局部炎症反应，介导CNP发生”。进一步实验拟采用敲低和过表达、抑制剂注射等体内体外实验探究CXCL12/CXCR4轴是通过LASP1/AKT信号通路调控Th1细胞趋化，介导CNP发生；利用免疫共沉淀、蛋白电泳等实验揭示CXCL12/CXCR4轴激活LAPS1/AKT通路的具体作用机制，为CNP的免疫治疗提供新的思路。

Chronic nonbacterial prostatitis (CNP) has a high incidence and is prone to relapse after treatment, which seriously affects the quality of life of patients, but the underlying mechanism has not yet been elucidated. Studies have found that local infiltration of Th1 cells causes the pathogenesis of CNP. In the preliminary studies, we identified and validated a critical CXCL12/CXCR4 axis based RNA-seq analysis of the CNP mouse model, and the axis mediates the pathogenesis of CNP by regulating lymphocyte chemotaxis. Studies reported that CXCR4 regulates the migration of inflammatory cells via activating LASP1/AKT signaling pathway, while the underlying mechanism remains unknown. Based on preliminary results and previous reports, we speculate that “the CXCL12/CXCR4 axis promotes the migration of Th1 cells to the prostate by activating the LASP1/AKT signaling pathway, subsequently, causing local inflammatory responses and mediating the pathogenesis of CNP”. Further experiments are designed to explore how the CXCL12/CXCR4 axis mediates the pathogenesis of CNP via the LASP1/AKT signaling pathway based on knockdown and overexpression, inhibitor injection and other in vivo and in vitro experiments; employing the co-immunoprecipitation, western blot and other experiments to reveal the specific mechanism of how CXCL12/CXCR4 axis activates the LAPS1/AKT pathway. Our study provides a novel inspiration for the immunotherapy of chronic nonbacterial prostatitis patients.